PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29746940-4 2018 RESULTS: Our results demonstrated that the NLRP3 inflammasome activation and cytokines production by DCs are dependent on ROS generation, endosome acidification, and K+ efflux and involve the Pb recognition by dectin-1 and Syk phosphorylation. Reactive Oxygen Species 122-125 NLR family pyrin domain containing 3 Homo sapiens 43-48 29475133-0 2018 Reactive oxygen species promote tubular injury in diabetic nephropathy: The role of the mitochondrial ros-txnip-nlrp3 biological axis. Reactive Oxygen Species 0-23 NLR family pyrin domain containing 3 Homo sapiens 112-117 29475133-0 2018 Reactive oxygen species promote tubular injury in diabetic nephropathy: The role of the mitochondrial ros-txnip-nlrp3 biological axis. Reactive Oxygen Species 102-105 NLR family pyrin domain containing 3 Homo sapiens 112-117 29475133-9 2018 These results suggest that mitochondrial ROS-TXNIP/NLRP3/IL-1beta axis activation is responsible for tubular oxidative injury, which can be ameliorated by MitoQ via the inhibition of mtROS overproduction. Reactive Oxygen Species 41-44 NLR family pyrin domain containing 3 Homo sapiens 51-56 29682582-0 2018 Vitamin D3 Protects against Diabetic Retinopathy by Inhibiting High-Glucose-Induced Activation of the ROS/TXNIP/NLRP3 Inflammasome Pathway. Reactive Oxygen Species 102-105 NLR family pyrin domain containing 3 Homo sapiens 112-117 29921379-5 2018 This finding highlights the possible molecular pathways involving NLRP3 activation for management of ROS and insulin IR. Reactive Oxygen Species 101-104 NLR family pyrin domain containing 3 Homo sapiens 66-71 29477360-3 2018 Here we demonstrated that the Nod-like receptor protein 3 (NLRP3) inflammasome is activated by mitochondrial reactive oxygen species (mROS) during I/R injury via direct interactions between the inflammasome and thioredoxin-interacting protein (TXNIP). Reactive Oxygen Species 109-132 NLR family pyrin domain containing 3 Homo sapiens 30-57 29477360-3 2018 Here we demonstrated that the Nod-like receptor protein 3 (NLRP3) inflammasome is activated by mitochondrial reactive oxygen species (mROS) during I/R injury via direct interactions between the inflammasome and thioredoxin-interacting protein (TXNIP). Reactive Oxygen Species 109-132 NLR family pyrin domain containing 3 Homo sapiens 59-64 29432801-10 2018 This study suggests that L. interrogans infection leads to reactive oxygen species (ROS)- and cathepsin B-dependent NLRP3 inflammasome activation, which subsequently mediates caspase-1 activation and IL-1beta and IL-18 release. Reactive Oxygen Species 59-82 NLR family pyrin domain containing 3 Homo sapiens 116-121 29743981-8 2018 Unfettered production of reactive oxygen species played a critical role in heme-mediated NLRP3 activation. Reactive Oxygen Species 25-48 NLR family pyrin domain containing 3 Homo sapiens 89-94 29374549-11 2018 AGEs induced HAEC injury by inducing reactive oxygen species -mediated NLRP3 inflammasome activation. Reactive Oxygen Species 37-60 NLR family pyrin domain containing 3 Homo sapiens 71-76 29374549-12 2018 Matrine recovered HAEC viability by inhibiting reactive oxygen species -mediated NLRP3 inflammasome activation. Reactive Oxygen Species 47-70 NLR family pyrin domain containing 3 Homo sapiens 81-86 29193391-5 2018 Moreover, NLRP3 siRNA transfection or treatment with inhibitors efficiently suppressed PA-induced pyroptosis, and pretreatment with total ROS scavenger or mtROS scavenger attenuated PA-induced NLRP3 inflammasome activation and subsequent pyroptosis. Reactive Oxygen Species 138-141 NLR family pyrin domain containing 3 Homo sapiens 193-198 29416034-8 2018 Further experiments revealed that the nicotine-NLRP3-ASC-pyroptosis pathway was activated by reactive oxygen species (ROS), since ROS scavenger (N-acetyl-cysteine, NAC) prevented endothelial cell pyroptosis. Reactive Oxygen Species 93-116 NLR family pyrin domain containing 3 Homo sapiens 47-52 29416034-0 2018 Nicotine promotes atherosclerosis via ROS-NLRP3-mediated endothelial cell pyroptosis. Reactive Oxygen Species 38-41 NLR family pyrin domain containing 3 Homo sapiens 42-47 29416034-8 2018 Further experiments revealed that the nicotine-NLRP3-ASC-pyroptosis pathway was activated by reactive oxygen species (ROS), since ROS scavenger (N-acetyl-cysteine, NAC) prevented endothelial cell pyroptosis. Reactive Oxygen Species 118-121 NLR family pyrin domain containing 3 Homo sapiens 47-52 29416034-8 2018 Further experiments revealed that the nicotine-NLRP3-ASC-pyroptosis pathway was activated by reactive oxygen species (ROS), since ROS scavenger (N-acetyl-cysteine, NAC) prevented endothelial cell pyroptosis. Reactive Oxygen Species 130-133 NLR family pyrin domain containing 3 Homo sapiens 47-52 29416034-9 2018 We conclude that pyroptosis is likely a cellular mechanism for the pro-atherosclerotic property of nicotine and stimulation of ROS to activate NLRP3 inflammasome is a signaling mechanism for nicotine-induced pyroptosis. Reactive Oxygen Species 127-130 NLR family pyrin domain containing 3 Homo sapiens 143-148 29107864-0 2018 TRPM2 dependence of ROS-induced NLRP3 activation in Alzheimer"s disease. Reactive Oxygen Species 20-23 NLR family pyrin domain containing 3 Homo sapiens 32-37 29257274-7 2018 In addition, the results demonstrated that miR-33 impaired mitochondrial oxygen consumption rates, resulting in the accumulation of cellular reactive oxygen species, which stimulated NLRP3 expression, caspase-1 activity and IL-1beta secretion. Reactive Oxygen Species 141-164 NLR family pyrin domain containing 3 Homo sapiens 183-188 29247992-4 2018 The NLRP3 inflammasome has also been shown to be regulated by mitochondrial reactive oxygen species and components of glycolysis, such as Hexokinase. Reactive Oxygen Species 76-99 NLR family pyrin domain containing 3 Homo sapiens 4-9 29107864-6 2018 According to this study, ROS produced from both mitochondria and NADPH oxidase was responsible for NLRP3 activation. Reactive Oxygen Species 25-28 NLR family pyrin domain containing 3 Homo sapiens 99-104 29107864-9 2018 Altogether, our findings supported the role of TRPM2 channel in ROS-induced NLRP3 activation in microglial cells through the exposure to Abeta. Reactive Oxygen Species 64-67 NLR family pyrin domain containing 3 Homo sapiens 76-81 30123891-6 2018 Excessive ROS can then result in activation of the NLRP3 inflammasome and secretion of IL-1 and IL-18 by caspase-1. Reactive Oxygen Species 10-13 NLR family pyrin domain containing 3 Homo sapiens 51-56 30014749-4 2018 Although reactive oxygen species (ROS) were reported to be involved in activation of NLRP3 inflammasome, we were hypothesized that IAPP could directly activate NLRP3 inflammasome, leading to islets beta-cell death. Reactive Oxygen Species 9-32 NLR family pyrin domain containing 3 Homo sapiens 85-90 30014749-4 2018 Although reactive oxygen species (ROS) were reported to be involved in activation of NLRP3 inflammasome, we were hypothesized that IAPP could directly activate NLRP3 inflammasome, leading to islets beta-cell death. Reactive Oxygen Species 34-37 NLR family pyrin domain containing 3 Homo sapiens 85-90 29263046-8 2017 In addition, we demonstrated that berberine may possibly reduce reactive oxygen species (ROS)-dependent NLRP3 inflammasome activation. Reactive Oxygen Species 64-87 NLR family pyrin domain containing 3 Homo sapiens 104-109 29312598-6 2017 In the present study, we demonstrated that IL-22 promoting IL-1beta secretion from keratinocytes via the Reactive oxygen species (ROS)-NOD-like receptor family, pyrin domain containing 3 (NLRP3)-caspase-1 pathway. Reactive Oxygen Species 105-128 NLR family pyrin domain containing 3 Homo sapiens 188-193 29312598-6 2017 In the present study, we demonstrated that IL-22 promoting IL-1beta secretion from keratinocytes via the Reactive oxygen species (ROS)-NOD-like receptor family, pyrin domain containing 3 (NLRP3)-caspase-1 pathway. Reactive Oxygen Species 130-133 NLR family pyrin domain containing 3 Homo sapiens 188-193 29255148-4 2017 This mechanism prevents collapse of mitochondrial membrane potential and the subsequent release of mitochondrial DNA and reactive oxygen species, thus preventing hyperactivation of NLRP3 inflammasome. Reactive Oxygen Species 121-144 NLR family pyrin domain containing 3 Homo sapiens 181-186 29263046-8 2017 In addition, we demonstrated that berberine may possibly reduce reactive oxygen species (ROS)-dependent NLRP3 inflammasome activation. Reactive Oxygen Species 89-92 NLR family pyrin domain containing 3 Homo sapiens 104-109 28849014-6 2017 It was found that Zn supplementation inhibited HG-induced NLRP3 inflammasome activation in the HPMCs by attenuating ROS production. Reactive Oxygen Species 116-119 NLR family pyrin domain containing 3 Homo sapiens 58-63 28849014-8 2017 These results indicated that Zn inhibited NLRP3 inflammasome activation in the HG-treated HPMCs by activating the Nrf2 antioxidant pathway and reducing the production of ROS. Reactive Oxygen Species 170-173 NLR family pyrin domain containing 3 Homo sapiens 42-47 28779175-3 2017 Here we show that chloride intracellular channels (CLIC) act downstream of the potassium efflux-mitochondrial reactive oxygen species (ROS) axis to promote NLRP3 inflammasome activation. Reactive Oxygen Species 110-133 NLR family pyrin domain containing 3 Homo sapiens 156-161 28870124-11 2017 The ZnO-NPs induced the activation of the NLRP3 inflammasome in A549 cells, which might be via a ROS-NF-kappaB-NLRP3 signaling pathway. Reactive Oxygen Species 97-100 NLR family pyrin domain containing 3 Homo sapiens 42-47 28870124-11 2017 The ZnO-NPs induced the activation of the NLRP3 inflammasome in A549 cells, which might be via a ROS-NF-kappaB-NLRP3 signaling pathway. Reactive Oxygen Species 97-100 NLR family pyrin domain containing 3 Homo sapiens 111-116 28870124-0 2017 Reactive oxygen species trigger NF-kappaB-mediated NLRP3 inflammasome activation induced by zinc oxide nanoparticles in A549 cells. Reactive Oxygen Species 0-23 NLR family pyrin domain containing 3 Homo sapiens 51-56 28779175-3 2017 Here we show that chloride intracellular channels (CLIC) act downstream of the potassium efflux-mitochondrial reactive oxygen species (ROS) axis to promote NLRP3 inflammasome activation. Reactive Oxygen Species 135-138 NLR family pyrin domain containing 3 Homo sapiens 156-161 28779175-4 2017 NLRP3 agonists induce potassium efflux, which causes mitochondrial damage and ROS production. Reactive Oxygen Species 78-81 NLR family pyrin domain containing 3 Homo sapiens 0-5 28779175-5 2017 Mitochondrial ROS then induces the translocation of CLICs to the plasma membrane for the induction of chloride efflux to promote NEK7-NLRP3 interaction, inflammasome assembly, caspase-1 activation, and IL-1beta secretion. Reactive Oxygen Species 14-17 NLR family pyrin domain containing 3 Homo sapiens 134-139 28790925-3 2017 ROS may promote the activation of nucleotide-binding oligomerization domain like receptor (NLR) pyrin domain containing 3 (NLRP3) inflammasome, a novel regulator of inflammation and cell death, by nuclear factor-kB (NF-kappaB) and thioredoxin interacting/inhibiting protein (TXNIP). Reactive Oxygen Species 0-3 NLR family pyrin domain containing 3 Homo sapiens 123-128 28004443-0 2017 Amyloid beta induces NLRP3 inflammasome activation in retinal pigment epithelial cells via NADPH oxidase- and mitochondria-dependent ROS production. Reactive Oxygen Species 133-136 NLR family pyrin domain containing 3 Homo sapiens 21-26 28224704-6 2017 Using NP cells established from healthy tissues, our in vitro study revealed that AGEs induced an inflammatory response in NP cells and a degenerative phenotype in a NLRP3-inflammasome-dependent manner related to the receptor for AGEs (RAGE)/NF-kappaB pathway and mitochondrial damage induced by mitochondrial reactive oxygen species (mtROS) generation, mitochondrial permeability transition pore (mPTP) activation and calcium mobilization. Reactive Oxygen Species 310-333 NLR family pyrin domain containing 3 Homo sapiens 166-171 28238526-6 2017 Reactive oxygen species-induced mitochondrial DNA oxidative damage and BRCC36 deubiquitinating activity provide a missing link and mechanism by which innate immunity responds to environmental stress via caspase-8-involved NLRP3/NLRP6 inflammasomes. Reactive Oxygen Species 0-23 NLR family pyrin domain containing 3 Homo sapiens 222-227 28004443-3 2017 In this study, we investigated the involvement of NADPH oxidase- and mitochondria-derived reactive oxygen species (ROS) in the process of Abeta1-40 -induced NLRP3 inflammasome activation in LPS-primed ARPE-19 cells. Reactive Oxygen Species 90-113 NLR family pyrin domain containing 3 Homo sapiens 157-162 28004443-3 2017 In this study, we investigated the involvement of NADPH oxidase- and mitochondria-derived reactive oxygen species (ROS) in the process of Abeta1-40 -induced NLRP3 inflammasome activation in LPS-primed ARPE-19 cells. Reactive Oxygen Species 115-118 NLR family pyrin domain containing 3 Homo sapiens 157-162 28004443-5 2017 Furthermore, the inductive effect of Abeta1-40 on NLRP3 inflammasome activation was mediated in a manner dependent on NADPH oxidase- and mitochondria-derived ROS. Reactive Oxygen Species 158-161 NLR family pyrin domain containing 3 Homo sapiens 50-55 28064010-0 2017 Vascular endothelial cells senescence is associated with NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation via reactive oxygen species (ROS)/thioredoxin-interacting protein (TXNIP) pathway. Reactive Oxygen Species 144-167 NLR family pyrin domain containing 3 Homo sapiens 109-114 28027970-0 2017 HBV inhibits LPS-induced NLRP3 inflammasome activation and IL-1beta production via suppressing the NF-kappaB pathway and ROS production. Reactive Oxygen Species 121-124 NLR family pyrin domain containing 3 Homo sapiens 25-30 28027970-10 2017 CONCLUSIONS: HBeAg inhibits LPS-induced NLRP3 inflammasome activation and IL-1beta production via suppressing NF-kappaB pathway and ROS production. Reactive Oxygen Species 132-135 NLR family pyrin domain containing 3 Homo sapiens 40-45 28027970-12 2017 LAY SUMMARY: HBeAg suppresses LPS-induced NLRP3 inflammasome activation and IL-1beta production in two ways, one is to repress NLRP3 and pro-IL-1beta expression via inhibiting NF-kappaB phosphorylation, and the other is to repress caspase-1 activation and IL-1beta maturation via inhibiting ROS production. Reactive Oxygen Species 291-294 NLR family pyrin domain containing 3 Homo sapiens 42-47 26961545-7 2017 The presence of ATP during TLR4 activation leads to NLRP3 inflammasome activation and caspase-1-mediated IL-1beta secretion which was inhibited during CD40 activation, accompanied with inhibition of ERK1/2 and reactive oxygen species (ROS), and elevation in p38 MAPK phosphorylation. Reactive Oxygen Species 210-233 NLR family pyrin domain containing 3 Homo sapiens 52-57 26961545-7 2017 The presence of ATP during TLR4 activation leads to NLRP3 inflammasome activation and caspase-1-mediated IL-1beta secretion which was inhibited during CD40 activation, accompanied with inhibition of ERK1/2 and reactive oxygen species (ROS), and elevation in p38 MAPK phosphorylation. Reactive Oxygen Species 235-238 NLR family pyrin domain containing 3 Homo sapiens 52-57 28087670-4 2017 Endoplasmic reticulum-loaded plant lectins then triggered Ca2+ release and mitochondrial damage, and inhibition of Ca2+ release and mitochondrial reactive oxygen species by chemical inhibitors significantly suppressed NLRP3 inflammasome activation. Reactive Oxygen Species 146-169 NLR family pyrin domain containing 3 Homo sapiens 218-223 28064010-0 2017 Vascular endothelial cells senescence is associated with NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation via reactive oxygen species (ROS)/thioredoxin-interacting protein (TXNIP) pathway. Reactive Oxygen Species 169-172 NLR family pyrin domain containing 3 Homo sapiens 109-114 28064010-6 2017 NLRP3 inflammasome was found to mediate IL-1beta secretion through the production of ROS (reactive oxygen species) during the senescence of endothelial cells. Reactive Oxygen Species 85-88 NLR family pyrin domain containing 3 Homo sapiens 0-5 28064010-6 2017 NLRP3 inflammasome was found to mediate IL-1beta secretion through the production of ROS (reactive oxygen species) during the senescence of endothelial cells. Reactive Oxygen Species 90-113 NLR family pyrin domain containing 3 Homo sapiens 0-5 28064010-7 2017 Furthermore, the association of TXNIP (thioredoxin-interacting protein) with NLRP3 induced by ROS promoted NLRP3 inflammasome activation in senescent endothelial cells. Reactive Oxygen Species 94-97 NLR family pyrin domain containing 3 Homo sapiens 77-82 28064010-7 2017 Furthermore, the association of TXNIP (thioredoxin-interacting protein) with NLRP3 induced by ROS promoted NLRP3 inflammasome activation in senescent endothelial cells. Reactive Oxygen Species 94-97 NLR family pyrin domain containing 3 Homo sapiens 107-112 27845246-7 2017 Palmitate-induced NLRP3 inflammasome activation in LPS-primed cardiac fibroblasts was associated with reduced AMPK activity, mitochondrial reactive oxygen species production and mitochondrial dysfunction. Reactive Oxygen Species 139-162 NLR family pyrin domain containing 3 Homo sapiens 18-23 28057759-7 2017 However, both NLRP3 depletion and inhibition of K+ efflux mitigated abacavir-induced mitochondrial reactive oxygen species production and cytotoxicity, suggesting that these processes were secondary to NLRP3 activation. Reactive Oxygen Species 99-122 NLR family pyrin domain containing 3 Homo sapiens 14-19 27751866-6 2017 Inflammasome activation was initiated by mitochondrial reactive oxygen species production triggered by chromium (VI), as indicated by sensitivity to treatment with the ROS scavenger N-acetyl cysteine and a coinciding failure of K+ efflux, caspase-1, or NLRP3 inhibition to prevent mitochondrial reactive oxygen species accumulation. Reactive Oxygen Species 55-78 NLR family pyrin domain containing 3 Homo sapiens 253-258 28084571-9 2017 Blockade of LOX-1 or NLRP3 inflammasome with specific siRNAs reduced xanthine oxidase-induced foam cell formation, ROS generation and activation of NLRP3 and downstream signals. Reactive Oxygen Species 115-118 NLR family pyrin domain containing 3 Homo sapiens 21-26 28084571-13 2017 Xanthine oxidase stimulates LOX-1 expression on the cell membrane of macrophages and vascular smooth muscle cells (VSMCs) and increases generation of ROS, which activate NLRP3 inflammasome and downstream pro-inflammatory mediators such as Caspase-1, IL-1beta and IL-18. Reactive Oxygen Species 150-153 NLR family pyrin domain containing 3 Homo sapiens 170-175 28110709-5 2017 Mitochondrial reactive oxygen species in turn activate the NLRP3 inflammasome, allowing increased IL-1beta processing and secretion, which likely underlies both chromium(VI)-induced cutaneous toxicity and sensitization. Reactive Oxygen Species 14-37 NLR family pyrin domain containing 3 Homo sapiens 59-64 27779191-4 2016 Intriguingly, 25-HC, but not VLCFA, promotes robust NLRP3 inflammasome assembly and activation via potassium efflux-, mitochondrial reactive oxygen species (ROS)- and liver X receptor (LXR)-mediated pathways. Reactive Oxygen Species 132-155 NLR family pyrin domain containing 3 Homo sapiens 52-57 28854426-0 2017 Autophagy Inhibition Contributes to ROS-Producing NLRP3-Dependent Inflammasome Activation and Cytokine Secretion in High Glucose-Induced Macrophages. Reactive Oxygen Species 36-39 NLR family pyrin domain containing 3 Homo sapiens 50-55 28854426-12 2017 Autophagy inhibition and ROS generation play an essential role in high glucose-induced NLRP3 inflammasome activation and cytokine secretion in macrophages. Reactive Oxygen Species 25-28 NLR family pyrin domain containing 3 Homo sapiens 87-92 27737891-6 2016 Notably, knockdown of NLRP3 or caspase-1, neutralization of S100A9, and pharmacologic inhibition of NLRP3 or NOX suppress pyroptosis, ROS generation, and nuclear beta-catenin in MDSs and are sufficient to restore effective hematopoiesis. Reactive Oxygen Species 134-137 NLR family pyrin domain containing 3 Homo sapiens 22-27 27737891-6 2016 Notably, knockdown of NLRP3 or caspase-1, neutralization of S100A9, and pharmacologic inhibition of NLRP3 or NOX suppress pyroptosis, ROS generation, and nuclear beta-catenin in MDSs and are sufficient to restore effective hematopoiesis. Reactive Oxygen Species 134-137 NLR family pyrin domain containing 3 Homo sapiens 100-105 27833015-0 2016 Trimethylamine N-oxide induces inflammation and endothelial dysfunction in human umbilical vein endothelial cells via activating ROS-TXNIP-NLRP3 inflammasome. Reactive Oxygen Species 129-132 NLR family pyrin domain containing 3 Homo sapiens 139-144 27833015-3 2016 Moreover, thioredoxin-interactive protein (TXNIP) activation is a key event linked to NLRP3 inflammasome via reactive oxygen species (ROS). Reactive Oxygen Species 109-132 NLR family pyrin domain containing 3 Homo sapiens 86-91 27833015-3 2016 Moreover, thioredoxin-interactive protein (TXNIP) activation is a key event linked to NLRP3 inflammasome via reactive oxygen species (ROS). Reactive Oxygen Species 134-137 NLR family pyrin domain containing 3 Homo sapiens 86-91 27833015-8 2016 Taken together, our results firstly reveal that TMAO induces inflammation and endothelial dysfunction via activating ROS-TXNIP-NLRP3 inflammasome, suggest a likely mechanism for TMAO-dependent enhancement in atherosclerosis and cardiovascular risks. Reactive Oxygen Species 117-120 NLR family pyrin domain containing 3 Homo sapiens 127-132 27600432-5 2016 Mitochondrial dysfunction acts upstream of NLRP3 activation by providing reactive oxygen species (ROS) to trigger NLRP3 oligomerization or by inducing alpha-tubulin acetylation to relocate mitochondria to the proximity of NLRP3. Reactive Oxygen Species 73-96 NLR family pyrin domain containing 3 Homo sapiens 43-48 27600432-5 2016 Mitochondrial dysfunction acts upstream of NLRP3 activation by providing reactive oxygen species (ROS) to trigger NLRP3 oligomerization or by inducing alpha-tubulin acetylation to relocate mitochondria to the proximity of NLRP3. Reactive Oxygen Species 98-101 NLR family pyrin domain containing 3 Homo sapiens 43-48 27600432-5 2016 Mitochondrial dysfunction acts upstream of NLRP3 activation by providing reactive oxygen species (ROS) to trigger NLRP3 oligomerization or by inducing alpha-tubulin acetylation to relocate mitochondria to the proximity of NLRP3. Reactive Oxygen Species 98-101 NLR family pyrin domain containing 3 Homo sapiens 114-119 27600432-5 2016 Mitochondrial dysfunction acts upstream of NLRP3 activation by providing reactive oxygen species (ROS) to trigger NLRP3 oligomerization or by inducing alpha-tubulin acetylation to relocate mitochondria to the proximity of NLRP3. Reactive Oxygen Species 98-101 NLR family pyrin domain containing 3 Homo sapiens 114-119 27538510-5 2017 Several molecular signaling pathways are shown to mediate the activation of the NLRP3 inflammasome, and they are related to the modifications in K+ efflux, increased lysosome leakage and activation of cathepsin B or enhanced reactive oxygen species (ROS) production. Reactive Oxygen Species 225-248 NLR family pyrin domain containing 3 Homo sapiens 80-85 27538510-5 2017 Several molecular signaling pathways are shown to mediate the activation of the NLRP3 inflammasome, and they are related to the modifications in K+ efflux, increased lysosome leakage and activation of cathepsin B or enhanced reactive oxygen species (ROS) production. Reactive Oxygen Species 250-253 NLR family pyrin domain containing 3 Homo sapiens 80-85 27614220-9 2016 In addition, NA inhibited NLRP3 inflammasome activation partly through suppression of ROS. Reactive Oxygen Species 86-89 NLR family pyrin domain containing 3 Homo sapiens 26-31 27614220-10 2016 Taken together, these findings indicate that NA is able to regulate the activation of NLRP3 inflammasome in HUVECs, which may be partly mediated by SIRT1 and ROS. Reactive Oxygen Species 158-161 NLR family pyrin domain containing 3 Homo sapiens 86-91 27779191-4 2016 Intriguingly, 25-HC, but not VLCFA, promotes robust NLRP3 inflammasome assembly and activation via potassium efflux-, mitochondrial reactive oxygen species (ROS)- and liver X receptor (LXR)-mediated pathways. Reactive Oxygen Species 157-160 NLR family pyrin domain containing 3 Homo sapiens 52-57 26959386-0 2016 Trichomonas vaginalis induces IL-1beta production in a human prostate epithelial cell line by activating the NLRP3 inflammasome via reactive oxygen species and potassium ion efflux. Reactive Oxygen Species 132-155 NLR family pyrin domain containing 3 Homo sapiens 109-114 27300134-13 2016 In conclusion, palmitic acid caused activation of NLRP3 inflammasomes and inflammatory responses, inducing IL-1beta, IL-6, and IL-8 secretion, which is associated with ROS generation, in human Sw.71 placental cells. Reactive Oxygen Species 168-171 NLR family pyrin domain containing 3 Homo sapiens 50-55 27731349-7 2016 These results provided a mechanistic linking between TRPM2-mediated Ca2+ influx and p47 phox signaling to induce excess ROS production and TXNIP-mediated NLRP3 inflammasome activation under HG, and suggested that TRPM2 represented a potential target for alleviating NLRP3 inflammasome activation related to hyperglycemia-induced oxidative stress in Type 2 diabetes Mellitus (T2DM). Reactive Oxygen Species 120-123 NLR family pyrin domain containing 3 Homo sapiens 266-271 26959386-14 2016 CONCLUSIONS: T. vaginalis induces the formation of the NLRP3 inflammasome in human prostate epithelial cells via ROS and potassium ion efflux, and this results in IL-1beta production. Reactive Oxygen Species 113-116 NLR family pyrin domain containing 3 Homo sapiens 55-60 27379212-5 2016 Specifically, the alarmin S100A9 and/or founder gene mutations trigger pyroptosis through the generation of reactive oxygen species leading to assembly and activation of the redox-sensitive NLRP3 inflammasome and beta-catenin, assuring propagation of the MDS clone. Reactive Oxygen Species 108-131 NLR family pyrin domain containing 3 Homo sapiens 190-195 25829326-3 2016 Urate-induced inflammasome pathway is comprised of urate crystal uptake into intracellular lysosomes and subsequent lysosomal rupture with mitochondrial reactive oxygen species (ROS) production, which activates the NLRP3 inflammasome. Reactive Oxygen Species 178-181 NLR family pyrin domain containing 3 Homo sapiens 215-220 26825654-0 2016 The role of Resveratrol-induced mitophagy/autophagy in peritoneal mesothelial cells inflammatory injury via NLRP3 inflammasome activation triggered by mitochondrial ROS. Reactive Oxygen Species 165-168 NLR family pyrin domain containing 3 Homo sapiens 108-113 26825654-8 2016 Taken together, this study may provide a potential therapeutic strategy for peritoneal inflammatory injury via NLRP3 inflammasome activation triggered by mitochondrial ROS. Reactive Oxygen Species 168-171 NLR family pyrin domain containing 3 Homo sapiens 111-116 25829326-3 2016 Urate-induced inflammasome pathway is comprised of urate crystal uptake into intracellular lysosomes and subsequent lysosomal rupture with mitochondrial reactive oxygen species (ROS) production, which activates the NLRP3 inflammasome. Reactive Oxygen Species 153-176 NLR family pyrin domain containing 3 Homo sapiens 215-220 26728324-3 2016 The NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, being activated by reactive oxygen species (ROS), is identified as a novel mechanism of liver fibrosis. Reactive Oxygen Species 96-119 NLR family pyrin domain containing 3 Homo sapiens 56-61 26728324-3 2016 The NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, being activated by reactive oxygen species (ROS), is identified as a novel mechanism of liver fibrosis. Reactive Oxygen Species 121-124 NLR family pyrin domain containing 3 Homo sapiens 56-61 26728324-12 2016 INNOVATION AND CONCLUSIONS: Ang-(1-7) improved liver fibrosis by regulating NLRP3 inflammasome activation induced by Ang II-mediated ROS via redox balance modulation. Reactive Oxygen Species 133-136 NLR family pyrin domain containing 3 Homo sapiens 76-81 26809137-8 2016 Accordingly, pre-treatment with mtROS scavenger or total ROS scavenger reduced Cd-induced activation of NLRP3 inflammasome and pyroptotic cell death. Reactive Oxygen Species 34-37 NLR family pyrin domain containing 3 Homo sapiens 104-109 26901245-5 2016 Further experiments showed that K(+) efflux, reactive oxygen species (ROS) production, and mitochondrial DNA damage may be involved in NLRP3 inflammasome activation mediated by TCBQ. Reactive Oxygen Species 45-68 NLR family pyrin domain containing 3 Homo sapiens 135-140 26901245-5 2016 Further experiments showed that K(+) efflux, reactive oxygen species (ROS) production, and mitochondrial DNA damage may be involved in NLRP3 inflammasome activation mediated by TCBQ. Reactive Oxygen Species 70-73 NLR family pyrin domain containing 3 Homo sapiens 135-140 26825654-3 2016 Exposure of HPMCs to high glucose-based PD solutions resulted in ROS production, which can trigger NLRP3 activation, leading to IL-1beta secretion. Reactive Oxygen Species 65-68 NLR family pyrin domain containing 3 Homo sapiens 99-104 26831644-3 2016 Metaflammation is initiated by the activation of the NOD-like receptor (NLR), leucine-rich repeat, pyrin domaincontaining 3 (NLRP3) gene by mitochondrial reactive oxygen species (ROS). Reactive Oxygen Species 154-177 NLR family pyrin domain containing 3 Homo sapiens 125-130 26830368-13 2016 The mechanism of IL-17A-triggered NLRP3 activation and subsequent IL-1beta secretion was found to involve the generation of reactive oxygen species. Reactive Oxygen Species 124-147 NLR family pyrin domain containing 3 Homo sapiens 34-39 26831644-3 2016 Metaflammation is initiated by the activation of the NOD-like receptor (NLR), leucine-rich repeat, pyrin domaincontaining 3 (NLRP3) gene by mitochondrial reactive oxygen species (ROS). Reactive Oxygen Species 179-182 NLR family pyrin domain containing 3 Homo sapiens 125-130 27127546-0 2016 ROS-Mediated NLRP3 Inflammasome Activation in Brain, Heart, Kidney, and Testis Ischemia/Reperfusion Injury. Reactive Oxygen Species 0-3 NLR family pyrin domain containing 3 Homo sapiens 13-18 26881256-0 2016 High Glucose and Lipopolysaccharide Prime NLRP3 Inflammasome via ROS/TXNIP Pathway in Mesangial Cells. Reactive Oxygen Species 65-68 NLR family pyrin domain containing 3 Homo sapiens 42-47 26881256-4 2016 This study observed the expression of NLRP3 inflammasome signaling stimulated by high glucose, lipopolysaccharide, and reactive oxygen species (ROS) inhibitor N-acetyl-L-cysteine in glomerular mesangial cells, aiming to elucidate the mechanism by which the NLRP3 inflammasome signaling pathway may contribute to diabetic nephropathy. Reactive Oxygen Species 119-142 NLR family pyrin domain containing 3 Homo sapiens 38-43 26881256-4 2016 This study observed the expression of NLRP3 inflammasome signaling stimulated by high glucose, lipopolysaccharide, and reactive oxygen species (ROS) inhibitor N-acetyl-L-cysteine in glomerular mesangial cells, aiming to elucidate the mechanism by which the NLRP3 inflammasome signaling pathway may contribute to diabetic nephropathy. Reactive Oxygen Species 119-142 NLR family pyrin domain containing 3 Homo sapiens 257-262 26881256-4 2016 This study observed the expression of NLRP3 inflammasome signaling stimulated by high glucose, lipopolysaccharide, and reactive oxygen species (ROS) inhibitor N-acetyl-L-cysteine in glomerular mesangial cells, aiming to elucidate the mechanism by which the NLRP3 inflammasome signaling pathway may contribute to diabetic nephropathy. Reactive Oxygen Species 144-147 NLR family pyrin domain containing 3 Homo sapiens 38-43 26881256-4 2016 This study observed the expression of NLRP3 inflammasome signaling stimulated by high glucose, lipopolysaccharide, and reactive oxygen species (ROS) inhibitor N-acetyl-L-cysteine in glomerular mesangial cells, aiming to elucidate the mechanism by which the NLRP3 inflammasome signaling pathway may contribute to diabetic nephropathy. Reactive Oxygen Species 144-147 NLR family pyrin domain containing 3 Homo sapiens 257-262 26881256-8 2016 Our results firstly reveal that high glucose and lipopolysaccharide activate ROS/TXNIP/ NLRP3/IL-1beta inflammasome signaling in glomerular mesangial cells, suggesting a mechanism by which inflammation may contribute to the development of diabetic nephropathy. Reactive Oxygen Species 77-80 NLR family pyrin domain containing 3 Homo sapiens 88-93 26540403-2 2016 Mitochondrial production of reactive oxygen species was recently linked to activation of an inflammatory redox sensor, the nod-like receptor family pyrin domain-containing 3 (NLRP3). Reactive Oxygen Species 28-51 NLR family pyrin domain containing 3 Homo sapiens 175-180 26355761-7 2016 Also, we found that homoplantaginin tightly controlled PA-induced reactive oxygen species to prevent nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome activation by suppressing reactive oxygen species-sensitive thioredoxin-interacting protein, NLRP3, and caspase-1. Reactive Oxygen Species 66-89 NLR family pyrin domain containing 3 Homo sapiens 101-142 26355761-7 2016 Also, we found that homoplantaginin tightly controlled PA-induced reactive oxygen species to prevent nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome activation by suppressing reactive oxygen species-sensitive thioredoxin-interacting protein, NLRP3, and caspase-1. Reactive Oxygen Species 66-89 NLR family pyrin domain containing 3 Homo sapiens 144-149 26355761-7 2016 Also, we found that homoplantaginin tightly controlled PA-induced reactive oxygen species to prevent nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome activation by suppressing reactive oxygen species-sensitive thioredoxin-interacting protein, NLRP3, and caspase-1. Reactive Oxygen Species 66-89 NLR family pyrin domain containing 3 Homo sapiens 257-262 26355761-7 2016 Also, we found that homoplantaginin tightly controlled PA-induced reactive oxygen species to prevent nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome activation by suppressing reactive oxygen species-sensitive thioredoxin-interacting protein, NLRP3, and caspase-1. Reactive Oxygen Species 190-213 NLR family pyrin domain containing 3 Homo sapiens 101-142 26355761-7 2016 Also, we found that homoplantaginin tightly controlled PA-induced reactive oxygen species to prevent nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome activation by suppressing reactive oxygen species-sensitive thioredoxin-interacting protein, NLRP3, and caspase-1. Reactive Oxygen Species 190-213 NLR family pyrin domain containing 3 Homo sapiens 144-149 26355761-7 2016 Also, we found that homoplantaginin tightly controlled PA-induced reactive oxygen species to prevent nucleotide-binding domain-like receptor 3 (NLRP3) inflammasome activation by suppressing reactive oxygen species-sensitive thioredoxin-interacting protein, NLRP3, and caspase-1. Reactive Oxygen Species 190-213 NLR family pyrin domain containing 3 Homo sapiens 257-262 27127546-5 2016 In particular, during I/R, ROS stimulate tissue inflammation and induce NLRP3 inflammasome activation. Reactive Oxygen Species 27-30 NLR family pyrin domain containing 3 Homo sapiens 72-77 27127546-7 2016 It was recently shown that NLRP3 might sense directly the presence of ROS produced by normal or malfunctioning mitochondria or indirectly by other activators of NLRP3. Reactive Oxygen Species 70-73 NLR family pyrin domain containing 3 Homo sapiens 27-32 27127546-7 2016 It was recently shown that NLRP3 might sense directly the presence of ROS produced by normal or malfunctioning mitochondria or indirectly by other activators of NLRP3. Reactive Oxygen Species 70-73 NLR family pyrin domain containing 3 Homo sapiens 161-166 25863775-15 2015 ATP promoted the generation of ROS and activated the NLRP3 inflammasome in a ROS-dependent manner. Reactive Oxygen Species 77-80 NLR family pyrin domain containing 3 Homo sapiens 53-58 25684031-7 2015 Furthermore, the low intracellular K(+) concentration in the cytosol triggers reactive oxygen species generation, which also induces the NLRP3 inflammasome. Reactive Oxygen Species 78-101 NLR family pyrin domain containing 3 Homo sapiens 137-142 26435000-6 2015 We used mitochondrial ROS (mROS) scavenger mitoTEMPO to demonstrate a role for mROS in NLRP3 inflammasome and programmed cell death induced by CPF. Reactive Oxygen Species 22-25 NLR family pyrin domain containing 3 Homo sapiens 87-92 26416893-1 2015 Mitochondrial dysfunction is considered crucial for NLRP3 inflammasome activation partly through its release of mitochondrial toxic products, such as mitochondrial reactive oxygen species (mROS)(2) and mitochondrial DNA (mtDNA). Reactive Oxygen Species 164-187 NLR family pyrin domain containing 3 Homo sapiens 52-57 26097125-6 2015 The results identify that a low-dose SWCNT treatment serves a protective function for the E. coli- and S. aureus-infected Caco-2 cells by negatively regulating mitochondrial reactive oxygen species-mediated NLRP3 inflammasome activation. Reactive Oxygen Species 174-197 NLR family pyrin domain containing 3 Homo sapiens 207-212 25834143-0 2015 Helicobacter pylori induces IL-1beta and IL-18 production in human monocytic cell line through activation of NLRP3 inflammasome via ROS signaling pathway. Reactive Oxygen Species 132-135 NLR family pyrin domain containing 3 Homo sapiens 109-114 25858687-0 2015 Lentinan exerts synergistic apoptotic effects with paclitaxel in A549 cells via activating ROS-TXNIP-NLRP3 inflammasome. Reactive Oxygen Species 91-94 NLR family pyrin domain containing 3 Homo sapiens 101-106 26114647-0 2015 PKC/ROS-Mediated NLRP3 Inflammasome Activation Is Attenuated by Leishmania Zinc-Metalloprotease during Infection. Reactive Oxygen Species 4-7 NLR family pyrin domain containing 3 Homo sapiens 17-22 25109682-3 2015 Reactive oxygen species (ROS) are major mediators of the NLRP3/IL-1beta interaction. Reactive Oxygen Species 0-23 NLR family pyrin domain containing 3 Homo sapiens 57-62 25109682-3 2015 Reactive oxygen species (ROS) are major mediators of the NLRP3/IL-1beta interaction. Reactive Oxygen Species 25-28 NLR family pyrin domain containing 3 Homo sapiens 57-62 26114647-10 2015 Leishmania-dependent suppression of IL-1beta secretion is accompanied by an inhibition of reactive oxygen species (ROS) production that has previously been shown to be associated with NLRP3 inflammasome activation. Reactive Oxygen Species 90-113 NLR family pyrin domain containing 3 Homo sapiens 184-189 26114647-10 2015 Leishmania-dependent suppression of IL-1beta secretion is accompanied by an inhibition of reactive oxygen species (ROS) production that has previously been shown to be associated with NLRP3 inflammasome activation. Reactive Oxygen Species 115-118 NLR family pyrin domain containing 3 Homo sapiens 184-189 25701684-0 2015 Reactive oxygen species activated NLRP3 inflammasomes initiate inflammation in hyperosmolarity stressed human corneal epithelial cells and environment-induced dry eye patients. Reactive Oxygen Species 0-23 NLR family pyrin domain containing 3 Homo sapiens 34-39 25330206-0 2015 Redox regulation of NLRP3 inflammasomes: ROS as trigger or effector? Reactive Oxygen Species 41-44 NLR family pyrin domain containing 3 Homo sapiens 20-25 25330206-5 2015 Several models have been developed to describe how NLRP3 inflammasomes are activated, including K(+) efflux, lysosome function, endoplasmic reticulum (ER) stress, intracellular calcium, ubiquitination, microRNAs, and, in particular, reactive oxygen species (ROS). Reactive Oxygen Species 233-256 NLR family pyrin domain containing 3 Homo sapiens 51-56 25330206-5 2015 Several models have been developed to describe how NLRP3 inflammasomes are activated, including K(+) efflux, lysosome function, endoplasmic reticulum (ER) stress, intracellular calcium, ubiquitination, microRNAs, and, in particular, reactive oxygen species (ROS). Reactive Oxygen Species 258-261 NLR family pyrin domain containing 3 Homo sapiens 51-56 25330206-6 2015 CRITICAL ISSUES: ROS may serve as a "kindling" or triggering factor to activate NLRP3 inflammasomes as well as "bonfire" or "effector" molecules, resulting in pathological processes. Reactive Oxygen Species 17-20 NLR family pyrin domain containing 3 Homo sapiens 80-85 25330206-7 2015 Increasing evidence seeks to understand how this spatiotemporal action of ROS occurs during NLRP3 inflammasome activation, which will be a major focus of this review. Reactive Oxygen Species 74-77 NLR family pyrin domain containing 3 Homo sapiens 92-97 25330206-8 2015 FUTURE DIRECTIONS: It is imperative to know how this dual action of ROS works during NLRP3 inflammation activation on different stimuli and what relevance such spatiotemporal redox regulation of NLRP3 inflammasomes has in cell or organ functions and possible human diseases. Reactive Oxygen Species 68-71 NLR family pyrin domain containing 3 Homo sapiens 85-90 25330206-8 2015 FUTURE DIRECTIONS: It is imperative to know how this dual action of ROS works during NLRP3 inflammation activation on different stimuli and what relevance such spatiotemporal redox regulation of NLRP3 inflammasomes has in cell or organ functions and possible human diseases. Reactive Oxygen Species 68-71 NLR family pyrin domain containing 3 Homo sapiens 195-200 25701684-2 2015 These immune reactions might be mediated by inflammasomes, macromolecular complexes mounted around the NLRP3 protein and can be activated by reactive oxygen species (ROS) over-generation. Reactive Oxygen Species 141-164 NLR family pyrin domain containing 3 Homo sapiens 103-108 25701684-2 2015 These immune reactions might be mediated by inflammasomes, macromolecular complexes mounted around the NLRP3 protein and can be activated by reactive oxygen species (ROS) over-generation. Reactive Oxygen Species 166-169 NLR family pyrin domain containing 3 Homo sapiens 103-108 25701684-3 2015 Hence in this study we determine whether: a) ROS activated NLRP3 inflammasomes mediate hyperosmotic stress-induced inflammation in human corneal epithelial cells (HCECs); b) the ROS-NLRP3-IL-1beta axis activation is associated with environment-induced DE. Reactive Oxygen Species 45-48 NLR family pyrin domain containing 3 Homo sapiens 59-64 25701684-3 2015 Hence in this study we determine whether: a) ROS activated NLRP3 inflammasomes mediate hyperosmotic stress-induced inflammation in human corneal epithelial cells (HCECs); b) the ROS-NLRP3-IL-1beta axis activation is associated with environment-induced DE. Reactive Oxygen Species 45-48 NLR family pyrin domain containing 3 Homo sapiens 182-187 25701684-3 2015 Hence in this study we determine whether: a) ROS activated NLRP3 inflammasomes mediate hyperosmotic stress-induced inflammation in human corneal epithelial cells (HCECs); b) the ROS-NLRP3-IL-1beta axis activation is associated with environment-induced DE. Reactive Oxygen Species 178-181 NLR family pyrin domain containing 3 Homo sapiens 59-64 25701684-3 2015 Hence in this study we determine whether: a) ROS activated NLRP3 inflammasomes mediate hyperosmotic stress-induced inflammation in human corneal epithelial cells (HCECs); b) the ROS-NLRP3-IL-1beta axis activation is associated with environment-induced DE. Reactive Oxygen Species 178-181 NLR family pyrin domain containing 3 Homo sapiens 182-187 25701684-14 2015 Taken together, NLRP3 mediated innate immune responses triggered by rises in ROS generation induce inflammation in hyperosmotic stressed HCECs. Reactive Oxygen Species 77-80 NLR family pyrin domain containing 3 Homo sapiens 16-21 25701684-15 2015 ROS-NLRP3-IL-1beta signaling pathway might play a priming role in environment-induced DE development. Reactive Oxygen Species 0-3 NLR family pyrin domain containing 3 Homo sapiens 4-9 25231464-9 2015 The mechanism of SAA-triggered NLRP3 activation and subsequent IL-1beta secretion was found to involve the generation of reactive oxygen species. Reactive Oxygen Species 121-144 NLR family pyrin domain containing 3 Homo sapiens 31-36 25800347-1 2015 Activation of the NLRP3 inflammasome by microbial ligands or tissue damage requires intracellular generation of reactive oxygen species (ROS). Reactive Oxygen Species 112-135 NLR family pyrin domain containing 3 Homo sapiens 18-23 25800347-1 2015 Activation of the NLRP3 inflammasome by microbial ligands or tissue damage requires intracellular generation of reactive oxygen species (ROS). Reactive Oxygen Species 137-140 NLR family pyrin domain containing 3 Homo sapiens 18-23 25327779-10 2015 Our findings suggest that reactive-oxygen-species-mediated activation of NLRP3 and AIM2 inflammasomes leads to I/R-induced inflammatory responses in which Kupffer cells play a crucial role. Reactive Oxygen Species 26-49 NLR family pyrin domain containing 3 Homo sapiens 73-78 26075098-3 2015 Recent studies have shown that mitochondrial production of ROS and inflammation may be closely linked through a redox sensor known as nod-like receptor pyrin domain-containing 3 (NLRP3). Reactive Oxygen Species 59-62 NLR family pyrin domain containing 3 Homo sapiens 134-177 26075098-3 2015 Recent studies have shown that mitochondrial production of ROS and inflammation may be closely linked through a redox sensor known as nod-like receptor pyrin domain-containing 3 (NLRP3). Reactive Oxygen Species 59-62 NLR family pyrin domain containing 3 Homo sapiens 179-184 26075098-4 2015 Upon sensing mitochondrial release of ROS, NLRP3 assembles the NLRP3 inflammasome, which releases caspase 1 to begin the inflammatory cascade. Reactive Oxygen Species 38-41 NLR family pyrin domain containing 3 Homo sapiens 43-48 26075098-4 2015 Upon sensing mitochondrial release of ROS, NLRP3 assembles the NLRP3 inflammasome, which releases caspase 1 to begin the inflammatory cascade. Reactive Oxygen Species 38-41 NLR family pyrin domain containing 3 Homo sapiens 63-68 25396345-2 2014 This results in excessive production of reactive oxygen species and subsequent activation of the NLRP3 inflammasome. Reactive Oxygen Species 40-63 NLR family pyrin domain containing 3 Homo sapiens 97-102 25281528-0 2014 Activation of the Nlrp3 inflammasome by mitochondrial reactive oxygen species: a novel mechanism of albumin-induced tubulointerstitial inflammation. Reactive Oxygen Species 54-77 NLR family pyrin domain containing 3 Homo sapiens 18-23 25281528-2 2014 In this study, we determined whether activation of the Nlrp3 inflammasome is involved in albuminuria induced-TIF and the underlying mechanisms of inflammasome activation by mitochondrial reactive oxygen species (mROS). Reactive Oxygen Species 187-210 NLR family pyrin domain containing 3 Homo sapiens 55-60 24820890-7 2014 The activation of the NLRP3 inflammasome by P. acnes was dependent on protease activity and reactive oxygen species generation. Reactive Oxygen Species 92-115 NLR family pyrin domain containing 3 Homo sapiens 22-27 25091898-6 2014 In addition, we critically evaluate controversial evidence suggesting a specific role for mitochondrial reactive oxygen species in the activation of the NLRP3 inflammasome, a multiprotein complex that mediates the production of IL-1beta and IL-18. Reactive Oxygen Species 104-127 NLR family pyrin domain containing 3 Homo sapiens 153-158 24217221-7 2014 Enhanced IL-1beta secretion depended on the activation of the NLRP3 inflammasome through a mechanism involving reactive oxygen species formation and activation of thioredoxin-interacting protein. Reactive Oxygen Species 111-134 NLR family pyrin domain containing 3 Homo sapiens 62-67 25225402-5 2014 The activation of NLRP3 by heme required spleen tyrosine kinase, NADPH oxidase-2, mitochondrial reactive oxygen species, and K(+) efflux, whereas it was independent of heme internalization, lysosomal damage, ATP release, the purinergic receptor P2X7, and cell death. Reactive Oxygen Species 96-119 NLR family pyrin domain containing 3 Homo sapiens 18-23 24307525-12 2014 Together, our results reveal that hMSCs inhibit NLRP3 inflammasome activation in macrophages primarily by secreting STC-1 in response to activated macrophages and thus by decreasing mitochondrial ROS. Reactive Oxygen Species 196-199 NLR family pyrin domain containing 3 Homo sapiens 48-53 24850149-7 2014 Alternative models for NLRP3 activation involve lysosomal destabilization and phagocytic NADPH oxidase and/or mitochondria-dependent reactive oxygen species (ROS) production. Reactive Oxygen Species 133-156 NLR family pyrin domain containing 3 Homo sapiens 23-28 24850149-7 2014 Alternative models for NLRP3 activation involve lysosomal destabilization and phagocytic NADPH oxidase and/or mitochondria-dependent reactive oxygen species (ROS) production. Reactive Oxygen Species 158-161 NLR family pyrin domain containing 3 Homo sapiens 23-28 24307525-0 2014 Mesenchymal stem/stromal cells inhibit the NLRP3 inflammasome by decreasing mitochondrial reactive oxygen species. Reactive Oxygen Species 90-113 NLR family pyrin domain containing 3 Homo sapiens 43-48 24776598-6 2014 To study the LOX-1-NLRP3 inflammasome signalling, we performed studies using ROS inhibitors and an autophagy inducer, and found that both decreased the expression of NLRP3. Reactive Oxygen Species 77-80 NLR family pyrin domain containing 3 Homo sapiens 166-171 23278511-4 2013 Intracellular ROS have been implicated in NLRP3 inflammasome-mediated IL-1beta production, therefore, we aimed to study whether RWE influences the function of NLRP3 inflammasome. Reactive Oxygen Species 14-17 NLR family pyrin domain containing 3 Homo sapiens 42-47 24806599-7 2014 All tested haptens, but not irritants, can induce Syk activation, leading to both the CARD9/BCL10-dependent pro-IL-1 synthesis (signal1) and reactive oxygen species-mediated NLRP3 inflammasome activation (signal2), required for IL-1 secretion. Reactive Oxygen Species 141-164 NLR family pyrin domain containing 3 Homo sapiens 174-179 24357806-5 2013 The processing is induced by an increase in activity of caspase-1 and NOD-like receptor family, pyrin domain containing 3 (NLRP3) via mitochondrial reactive oxygen species (ROS) and partially via NADPH oxidase-induced ROS. Reactive Oxygen Species 148-171 NLR family pyrin domain containing 3 Homo sapiens 123-128 24357806-5 2013 The processing is induced by an increase in activity of caspase-1 and NOD-like receptor family, pyrin domain containing 3 (NLRP3) via mitochondrial reactive oxygen species (ROS) and partially via NADPH oxidase-induced ROS. Reactive Oxygen Species 173-176 NLR family pyrin domain containing 3 Homo sapiens 123-128 24357806-5 2013 The processing is induced by an increase in activity of caspase-1 and NOD-like receptor family, pyrin domain containing 3 (NLRP3) via mitochondrial reactive oxygen species (ROS) and partially via NADPH oxidase-induced ROS. Reactive Oxygen Species 218-221 NLR family pyrin domain containing 3 Homo sapiens 123-128 24089192-0 2013 Mitochondrial reactive oxygen species induces NLRP3-dependent lysosomal damage and inflammasome activation. Reactive Oxygen Species 14-37 NLR family pyrin domain containing 3 Homo sapiens 46-51 24048902-2 2013 How NLRP3 senses these various stimuli is still poorly understood, but mitochondria and mitochondrial reactive oxygen species have been proposed to play a critical role in NLRP3 activation. Reactive Oxygen Species 102-125 NLR family pyrin domain containing 3 Homo sapiens 4-9 24048902-2 2013 How NLRP3 senses these various stimuli is still poorly understood, but mitochondria and mitochondrial reactive oxygen species have been proposed to play a critical role in NLRP3 activation. Reactive Oxygen Species 102-125 NLR family pyrin domain containing 3 Homo sapiens 172-177 24048902-7 2013 Taken together, our results suggest that MAVS facilitates the recruitment of NLRP3 to the mitochondria and may enhance its oligomerization and activation by bringing it in close proximity to mitochondrial reactive oxygen species. Reactive Oxygen Species 205-228 NLR family pyrin domain containing 3 Homo sapiens 77-82 23954133-2 2013 All previously evaluated activators of the Nlrp3 inflammasome induce the generation of mitochondrial reactive oxygen species (ROS), suggesting a model in which ROS is a required upstream mediator of Nlrp3 inflammasome activation. Reactive Oxygen Species 101-124 NLR family pyrin domain containing 3 Homo sapiens 43-48 23954133-2 2013 All previously evaluated activators of the Nlrp3 inflammasome induce the generation of mitochondrial reactive oxygen species (ROS), suggesting a model in which ROS is a required upstream mediator of Nlrp3 inflammasome activation. Reactive Oxygen Species 101-124 NLR family pyrin domain containing 3 Homo sapiens 199-204 23954133-2 2013 All previously evaluated activators of the Nlrp3 inflammasome induce the generation of mitochondrial reactive oxygen species (ROS), suggesting a model in which ROS is a required upstream mediator of Nlrp3 inflammasome activation. Reactive Oxygen Species 126-129 NLR family pyrin domain containing 3 Homo sapiens 43-48 23954133-2 2013 All previously evaluated activators of the Nlrp3 inflammasome induce the generation of mitochondrial reactive oxygen species (ROS), suggesting a model in which ROS is a required upstream mediator of Nlrp3 inflammasome activation. Reactive Oxygen Species 126-129 NLR family pyrin domain containing 3 Homo sapiens 199-204 23954133-2 2013 All previously evaluated activators of the Nlrp3 inflammasome induce the generation of mitochondrial reactive oxygen species (ROS), suggesting a model in which ROS is a required upstream mediator of Nlrp3 inflammasome activation. Reactive Oxygen Species 160-163 NLR family pyrin domain containing 3 Homo sapiens 43-48 23954133-2 2013 All previously evaluated activators of the Nlrp3 inflammasome induce the generation of mitochondrial reactive oxygen species (ROS), suggesting a model in which ROS is a required upstream mediator of Nlrp3 inflammasome activation. Reactive Oxygen Species 160-163 NLR family pyrin domain containing 3 Homo sapiens 199-204 23954133-4 2013 The pathways for ROS-dependent and ROS-independent Nlrp3 activation converged upon mitochondrial dysfunction and specifically the mitochondrial lipid cardiolipin. Reactive Oxygen Species 17-20 NLR family pyrin domain containing 3 Homo sapiens 51-56 23954133-4 2013 The pathways for ROS-dependent and ROS-independent Nlrp3 activation converged upon mitochondrial dysfunction and specifically the mitochondrial lipid cardiolipin. Reactive Oxygen Species 35-38 NLR family pyrin domain containing 3 Homo sapiens 51-56 23977231-0 2013 S100A8 and S100A9 induce cytokine expression and regulate the NLRP3 inflammasome via ROS-dependent activation of NF-kappaB(1.). Reactive Oxygen Species 85-88 NLR family pyrin domain containing 3 Homo sapiens 62-67 23977231-7 2013 S100A8- and S100A9-mediated activation of NF-kappaB, the NLR family, pyrin domain-containing 3 (NLRP3) protein, and pro-IL-1beta expression was dependent on the generation of reactive oxygen species. Reactive Oxygen Species 175-198 NLR family pyrin domain containing 3 Homo sapiens 57-94 23977231-7 2013 S100A8- and S100A9-mediated activation of NF-kappaB, the NLR family, pyrin domain-containing 3 (NLRP3) protein, and pro-IL-1beta expression was dependent on the generation of reactive oxygen species. Reactive Oxygen Species 175-198 NLR family pyrin domain containing 3 Homo sapiens 96-101 24400125-7 2014 CONCLUSIONS: Our results indicate that HCV RNA activates the NLRP3 inflammasome in a ROS-dependent manner, and RIG-I is not required for this process. Reactive Oxygen Species 85-88 NLR family pyrin domain containing 3 Homo sapiens 61-66 23454144-6 2013 ROS are also involved in the activation of the NLRP3/NALP3 inflammasome, which is required to direct the proteolytic maturation of inflammatory cytokines such as IL-1beta and IL-18, which are all integral to the process of dendritic cells mobilization, migration and functional maturation. Reactive Oxygen Species 0-3 NLR family pyrin domain containing 3 Homo sapiens 47-52 23454144-6 2013 ROS are also involved in the activation of the NLRP3/NALP3 inflammasome, which is required to direct the proteolytic maturation of inflammatory cytokines such as IL-1beta and IL-18, which are all integral to the process of dendritic cells mobilization, migration and functional maturation. Reactive Oxygen Species 0-3 NLR family pyrin domain containing 3 Homo sapiens 53-58 24127597-4 2013 Recent studies indicate that the reactive oxygen species produced by mitochondrial respiration is critical for the activation of the NLRP3 inflammasome by monosodium urate, alum, and ATP. Reactive Oxygen Species 33-56 NLR family pyrin domain containing 3 Homo sapiens 133-138 23315075-9 2013 These findings provide new insights in lupus pathogenesis by demonstrating that self dsDNA together with its autoantibodies induces IL-1beta production from human monocytes by activating the NLRP3 inflammasome through inducing ROS synthesis and K(+) efflux, leading to the increased Th17 cell response. Reactive Oxygen Species 227-230 NLR family pyrin domain containing 3 Homo sapiens 191-196 23211828-14 2013 Interaction of TLR2/4 with their ligands PGN/LPS is involved in BD pathogenesis, possibly by the induction of IL-1beta through a ROS-NLRP3-dependent pathway. Reactive Oxygen Species 129-132 NLR family pyrin domain containing 3 Homo sapiens 133-138 23065753-5 2012 In tumour cells, AIM2 and RIG-I are required for IL-1beta induction by EBV genomic DNA and EBV-encoded small RNAs, respectively, while NLRP3 responds to extracellular ATP and reactive oxygen species. Reactive Oxygen Species 175-198 NLR family pyrin domain containing 3 Homo sapiens 135-140 23211828-0 2013 IL-1beta triggered by peptidoglycan and lipopolysaccharide through TLR2/4 and ROS-NLRP3 inflammasome-dependent pathways is involved in ocular Behcet"s disease. Reactive Oxygen Species 78-81 NLR family pyrin domain containing 3 Homo sapiens 82-87 22948162-9 2012 Our findings suggest that NLRP3 is activated by a two-step deubiquitination mechanism initiated by Toll-like receptor signaling and mitochondrial reactive oxygen species and further potentiated by ATP, which could explain how NLRP3 is activated by diverse danger signals. Reactive Oxygen Species 146-169 NLR family pyrin domain containing 3 Homo sapiens 26-31 22948162-9 2012 Our findings suggest that NLRP3 is activated by a two-step deubiquitination mechanism initiated by Toll-like receptor signaling and mitochondrial reactive oxygen species and further potentiated by ATP, which could explain how NLRP3 is activated by diverse danger signals. Reactive Oxygen Species 146-169 NLR family pyrin domain containing 3 Homo sapiens 226-231 22065079-8 2012 Asbestos induces cell necrosis, causing the release of HMGB1, which in turn may activate Nalp3 inflammasome, a process that is enhanced by asbestos-induced production of reactive oxygen species. Reactive Oxygen Species 170-193 NLR family pyrin domain containing 3 Homo sapiens 89-94 22411934-4 2012 Nod-like receptor 3 (NLRP3) can be activated by many danger signals, e.g. ROS, cathepsin B released from destabilized lysosomes and aggregated proteins, all of which evoke cellular stress and are involved in the aging process. Reactive Oxygen Species 74-77 NLR family pyrin domain containing 3 Homo sapiens 0-19 22411934-4 2012 Nod-like receptor 3 (NLRP3) can be activated by many danger signals, e.g. ROS, cathepsin B released from destabilized lysosomes and aggregated proteins, all of which evoke cellular stress and are involved in the aging process. Reactive Oxygen Species 74-77 NLR family pyrin domain containing 3 Homo sapiens 21-26 22446749-4 2012 Nod-like receptor protein 3 (NLRP3) is the major immune sensor for cellular stress signals, e.g., reactive oxygen species, ceramides, and cathepsin B. Reactive Oxygen Species 98-121 NLR family pyrin domain containing 3 Homo sapiens 0-27 22446749-4 2012 Nod-like receptor protein 3 (NLRP3) is the major immune sensor for cellular stress signals, e.g., reactive oxygen species, ceramides, and cathepsin B. Reactive Oxygen Species 98-121 NLR family pyrin domain containing 3 Homo sapiens 29-34 22796220-0 2012 Oxidized low-density lipoprotein induces secretion of interleukin-1beta by macrophages via reactive oxygen species-dependent NLRP3 inflammasome activation. Reactive Oxygen Species 91-114 NLR family pyrin domain containing 3 Homo sapiens 125-130 22796220-4 2012 Here we show that the phagocytosis of ox-LDL can induce human macrophages to secrete IL-1beta by activating the NLRP3 inflammasome, and we further show that the activation of the NLRP3 inflammasome is dependent on the generation of reactive oxygen species and is related to the cathepsin B pathway. Reactive Oxygen Species 232-255 NLR family pyrin domain containing 3 Homo sapiens 179-184 22623753-3 2012 The inhibition of Rac1 activation and ROS generation suppressed the activity of the Nod-like receptor (NLR) family, pyrin domain-containing 3 (NLRP3) inflammasome, which resulted in attenuated EAE pathogenicity. Reactive Oxygen Species 38-41 NLR family pyrin domain containing 3 Homo sapiens 143-148 21940680-6 2011 In turn, reactive oxygen species derived from NAD(P)H oxidase promote the association of thioredoxin-interacting protein with the nucleotide-binding oligomerization domain-like receptor protein NLRP3 and subsequently induce inflammasome activation and IL-1beta secretion from the EC. Reactive Oxygen Species 9-32 NLR family pyrin domain containing 3 Homo sapiens 194-199 21957307-6 2011 Activation of the NLRP3 inflammasome and secretion of IL-1beta was also dependent on the release of cathepsin B and production of reactive oxygen species (ROS). Reactive Oxygen Species 130-153 NLR family pyrin domain containing 3 Homo sapiens 18-23 21957307-6 2011 Activation of the NLRP3 inflammasome and secretion of IL-1beta was also dependent on the release of cathepsin B and production of reactive oxygen species (ROS). Reactive Oxygen Species 155-158 NLR family pyrin domain containing 3 Homo sapiens 18-23 21930705-9 2011 In addition, inhibitors of reactive oxygen species, cathepsin B, and K(+) efflux pathways, known to specifically influence NLRP3, substantially but not completely impair the Francisella-elicited IL-1beta response, suggesting the involvement of another inflammasome pathway. Reactive Oxygen Species 27-50 NLR family pyrin domain containing 3 Homo sapiens 123-128 21677136-0 2011 Cutting edge: reactive oxygen species inhibitors block priming, but not activation, of the NLRP3 inflammasome. Reactive Oxygen Species 14-37 NLR family pyrin domain containing 3 Homo sapiens 91-96 21800904-8 2011 Moreover, it was noted that CNT-induced NLRP3 inflammasome activation depended on reactive oxygen species (ROS) production, cathepsin B activity, P2X(7) receptor, and Src and Syk tyrosine kinases. Reactive Oxygen Species 82-105 NLR family pyrin domain containing 3 Homo sapiens 40-45 21800904-8 2011 Moreover, it was noted that CNT-induced NLRP3 inflammasome activation depended on reactive oxygen species (ROS) production, cathepsin B activity, P2X(7) receptor, and Src and Syk tyrosine kinases. Reactive Oxygen Species 107-110 NLR family pyrin domain containing 3 Homo sapiens 40-45 21677136-2 2011 Recently, production of reactive oxygen species (ROS) has been suggested to act as a common event upstream of the NLRP3 inflammasome machinery. Reactive Oxygen Species 24-47 NLR family pyrin domain containing 3 Homo sapiens 114-119 21677136-2 2011 Recently, production of reactive oxygen species (ROS) has been suggested to act as a common event upstream of the NLRP3 inflammasome machinery. Reactive Oxygen Species 49-52 NLR family pyrin domain containing 3 Homo sapiens 114-119 21677136-4 2011 Although we observe that NLRP3 inflammasome activation is unique among other known inflammasomes in its sensitivity to ROS inhibition, we have found that this phenomenon is attributable to the fact that NLRP3 strictly requires priming by a proinflammatory signal, a step that is blocked by ROS inhibitors. Reactive Oxygen Species 119-122 NLR family pyrin domain containing 3 Homo sapiens 25-30 21677136-4 2011 Although we observe that NLRP3 inflammasome activation is unique among other known inflammasomes in its sensitivity to ROS inhibition, we have found that this phenomenon is attributable to the fact that NLRP3 strictly requires priming by a proinflammatory signal, a step that is blocked by ROS inhibitors. Reactive Oxygen Species 119-122 NLR family pyrin domain containing 3 Homo sapiens 203-208 21677136-4 2011 Although we observe that NLRP3 inflammasome activation is unique among other known inflammasomes in its sensitivity to ROS inhibition, we have found that this phenomenon is attributable to the fact that NLRP3 strictly requires priming by a proinflammatory signal, a step that is blocked by ROS inhibitors. Reactive Oxygen Species 290-293 NLR family pyrin domain containing 3 Homo sapiens 25-30 21677136-4 2011 Although we observe that NLRP3 inflammasome activation is unique among other known inflammasomes in its sensitivity to ROS inhibition, we have found that this phenomenon is attributable to the fact that NLRP3 strictly requires priming by a proinflammatory signal, a step that is blocked by ROS inhibitors. Reactive Oxygen Species 290-293 NLR family pyrin domain containing 3 Homo sapiens 203-208 21677136-5 2011 Although these data do not exclude a general role for ROS production in the process of NLRP3-triggered inflammation, they would put ROS upstream of NLRP3 induction, but not activation. Reactive Oxygen Species 132-135 NLR family pyrin domain containing 3 Homo sapiens 148-153 21282379-1 2011 Reactive oxygen species (ROS) have an established role in inflammation and host defense, as they kill intracellular bacteria and have been shown to activate the NLRP3 inflammasome. Reactive Oxygen Species 0-23 NLR family pyrin domain containing 3 Homo sapiens 161-166 21282379-1 2011 Reactive oxygen species (ROS) have an established role in inflammation and host defense, as they kill intracellular bacteria and have been shown to activate the NLRP3 inflammasome. Reactive Oxygen Species 25-28 NLR family pyrin domain containing 3 Homo sapiens 161-166 20407038-3 2010 The precise mode of activation of the NLRP3 inflammasome is still elusive, but has been postulated to be mediated by reactive oxygen species (ROS) generated by an NADPH oxidase. Reactive Oxygen Species 142-145 NLR family pyrin domain containing 3 Homo sapiens 38-43 21124315-2 2011 Previous studies suggested that NLRP3 inflammasome activity is negatively regulated by autophagy and positively regulated by reactive oxygen species (ROS) derived from an uncharacterized organelle. Reactive Oxygen Species 125-148 NLR family pyrin domain containing 3 Homo sapiens 32-37 21124315-2 2011 Previous studies suggested that NLRP3 inflammasome activity is negatively regulated by autophagy and positively regulated by reactive oxygen species (ROS) derived from an uncharacterized organelle. Reactive Oxygen Species 150-153 NLR family pyrin domain containing 3 Homo sapiens 32-37 21124315-3 2011 Here we show that mitophagy/autophagy blockade leads to the accumulation of damaged, ROS-generating mitochondria, and this in turn activates the NLRP3 inflammasome. Reactive Oxygen Species 85-88 NLR family pyrin domain containing 3 Homo sapiens 145-150 20561679-0 2010 The effect of surface modification of amorphous silica particles on NLRP3 inflammasome mediated IL-1beta production, ROS production and endosomal rupture. Reactive Oxygen Species 117-120 NLR family pyrin domain containing 3 Homo sapiens 68-73 20632067-4 2011 XOD produces uric acid and reactive oxygen species, which could activate Nalp3 and therefore induce activation of caspase 1, known to convert inactive pro-IL-1beta into active IL-1beta. Reactive Oxygen Species 27-50 NLR family pyrin domain containing 3 Homo sapiens 73-78 20407038-3 2010 The precise mode of activation of the NLRP3 inflammasome is still elusive, but has been postulated to be mediated by reactive oxygen species (ROS) generated by an NADPH oxidase. Reactive Oxygen Species 117-140 NLR family pyrin domain containing 3 Homo sapiens 38-43 20168318-0 2010 NLRP3 inflammasome activation: The convergence of multiple signalling pathways on ROS production? Reactive Oxygen Species 82-85 NLR family pyrin domain containing 3 Homo sapiens 0-5 20421639-10 2010 Furthermore, our results suggest that the lysosomal cathepsin B protease, the formation of reactive oxygen species, and the efflux of potassium are needed for beta-glucan-induced NLRP3 inflammasome activation. Reactive Oxygen Species 91-114 NLR family pyrin domain containing 3 Homo sapiens 179-184 20168318-4 2010 In this Opinion article, we review the different signalling pathways that have been proposed to engage the NLRP3 inflammasome and suggest a model in which one of the crucial elements for NLRP3 activation is the generation of reactive oxygen species (ROS). Reactive Oxygen Species 225-248 NLR family pyrin domain containing 3 Homo sapiens 107-112 20168318-4 2010 In this Opinion article, we review the different signalling pathways that have been proposed to engage the NLRP3 inflammasome and suggest a model in which one of the crucial elements for NLRP3 activation is the generation of reactive oxygen species (ROS). Reactive Oxygen Species 225-248 NLR family pyrin domain containing 3 Homo sapiens 187-192 20168318-4 2010 In this Opinion article, we review the different signalling pathways that have been proposed to engage the NLRP3 inflammasome and suggest a model in which one of the crucial elements for NLRP3 activation is the generation of reactive oxygen species (ROS). Reactive Oxygen Species 250-253 NLR family pyrin domain containing 3 Homo sapiens 107-112 20168318-4 2010 In this Opinion article, we review the different signalling pathways that have been proposed to engage the NLRP3 inflammasome and suggest a model in which one of the crucial elements for NLRP3 activation is the generation of reactive oxygen species (ROS). Reactive Oxygen Species 250-253 NLR family pyrin domain containing 3 Homo sapiens 187-192 20075245-3 2010 In doing so, we integrate previously disparate disease-driving mechanisms for IL-1beta, ROS, and TXNIP in T2DM into one unifying model in which the NLRP3 inflammasome plays a central role. Reactive Oxygen Species 88-91 NLR family pyrin domain containing 3 Homo sapiens 148-153 34903138-2 2021 Damaged mitochondria release dangerous molecules such as reactive oxygen species (ROS), activating the NLRP3 inflammasome. Reactive Oxygen Species 57-80 NLR family pyrin domain containing 3 Homo sapiens 103-108 33763153-3 2021 NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome has been previously demonstrated to serve a role in obese asthma mediated by mitochondrial reactive oxygen species (mtROS). Reactive Oxygen Species 161-184 NLR family pyrin domain containing 3 Homo sapiens 0-48 33763153-3 2021 NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3) inflammasome has been previously demonstrated to serve a role in obese asthma mediated by mitochondrial reactive oxygen species (mtROS). Reactive Oxygen Species 161-184 NLR family pyrin domain containing 3 Homo sapiens 50-55 34688696-11 2022 Quercetin suppressed NLRP3 inflammasome activation by inhibiting ROS overproduction. Reactive Oxygen Species 65-68 NLR family pyrin domain containing 3 Homo sapiens 21-26 34903138-8 2021 The results indicate that SS-31 could inhibit NLRP3 inflammasome activation by limiting the production of mitochondrial ROS. Reactive Oxygen Species 120-123 NLR family pyrin domain containing 3 Homo sapiens 46-51 19439372-5 2009 Aluminum adjuvants activate NLRP3 by multiple mechanisms such as by causing damage and rupture of the phagolysosomes, generating reactive oxygen species, inducing K(+) efflux and via release from injured tissues of molecules that constitute danger-associated molecular patterns (DAMPs) such as uric acid and ATP. Reactive Oxygen Species 129-152 NLR family pyrin domain containing 3 Homo sapiens 28-33 19362020-6 2009 Mechanistically, NLRP3 inflammasome activation by the influenza virus was dependent on lysosomal maturation and reactive oxygen species (ROS). Reactive Oxygen Species 112-135 NLR family pyrin domain containing 3 Homo sapiens 17-22 19362020-6 2009 Mechanistically, NLRP3 inflammasome activation by the influenza virus was dependent on lysosomal maturation and reactive oxygen species (ROS). Reactive Oxygen Species 137-140 NLR family pyrin domain containing 3 Homo sapiens 17-22 18577586-7 2008 Activation of the Nalp3 inflammasome by silica required both an efflux of intracellular potassium and the generation of reactive oxygen species. Reactive Oxygen Species 120-143 NLR family pyrin domain containing 3 Homo sapiens 18-23 34965405-2 2022 ROS generation is known to activate NLRP3 (nucleotide-binding oligomerization domain-like receptor family, pyrin domain-cointaining 3) inflammasome, and is believed to be an important link between oxidative stress and inflammation, that is also related to cataract development. Reactive Oxygen Species 0-3 NLR family pyrin domain containing 3 Homo sapiens 36-41 34903138-2 2021 Damaged mitochondria release dangerous molecules such as reactive oxygen species (ROS), activating the NLRP3 inflammasome. Reactive Oxygen Species 82-85 NLR family pyrin domain containing 3 Homo sapiens 103-108 34988126-2 2021 Aging is linked to chronic sterile inflammation and high burden of reactive oxygen species (ROS), leading to activation of pattern recognition receptors (PRRs) such as Nlrp3 in vascular cells. Reactive Oxygen Species 67-90 NLR family pyrin domain containing 3 Homo sapiens 168-173 34988126-2 2021 Aging is linked to chronic sterile inflammation and high burden of reactive oxygen species (ROS), leading to activation of pattern recognition receptors (PRRs) such as Nlrp3 in vascular cells. Reactive Oxygen Species 92-95 NLR family pyrin domain containing 3 Homo sapiens 168-173 34899720-0 2021 SIRT1 Promotes M2 Microglia Polarization via Reducing ROS-Mediated NLRP3 Inflammasome Signaling After Subarachnoid Hemorrhage. Reactive Oxygen Species 54-57 NLR family pyrin domain containing 3 Homo sapiens 67-72 34899720-8 2021 In contrast, EX527 abated the upregulation of SIRT1 and reversed the inhibitory effects of SRT1720 on ROS-NLRP3 inflammasome activation and EBI. Reactive Oxygen Species 102-105 NLR family pyrin domain containing 3 Homo sapiens 106-111 34899720-11 2021 Altogether, these findings indicate that SRT1720, an SIRT1 agonist, can ameliorate EBI after SAH by shifting the microglial phenotype toward M2 via modulation of ROS-mediated NLRP3 inflammasome signaling. Reactive Oxygen Species 162-165 NLR family pyrin domain containing 3 Homo sapiens 175-180 34831052-4 2021 Furthermore, reactive oxygen species (ROS), act as an intermediate to activate NLRP3, contributing to subsequent inflammatory cascades and cell damage. Reactive Oxygen Species 13-36 NLR family pyrin domain containing 3 Homo sapiens 79-84 34238121-8 2021 In summary, acrolein induced cytotoxicity by ROS-mediated NLRP3 inflammasome activation, and ROS upregulates the level of autophagy to inhibit the NLRP3 inflammasome excessive activation, indicating the bidirectional role of ROS in acrolein-induced cellular inflammation. Reactive Oxygen Species 45-48 NLR family pyrin domain containing 3 Homo sapiens 58-63 34238121-8 2021 In summary, acrolein induced cytotoxicity by ROS-mediated NLRP3 inflammasome activation, and ROS upregulates the level of autophagy to inhibit the NLRP3 inflammasome excessive activation, indicating the bidirectional role of ROS in acrolein-induced cellular inflammation. Reactive Oxygen Species 93-96 NLR family pyrin domain containing 3 Homo sapiens 147-152 34238121-8 2021 In summary, acrolein induced cytotoxicity by ROS-mediated NLRP3 inflammasome activation, and ROS upregulates the level of autophagy to inhibit the NLRP3 inflammasome excessive activation, indicating the bidirectional role of ROS in acrolein-induced cellular inflammation. Reactive Oxygen Species 225-228 NLR family pyrin domain containing 3 Homo sapiens 147-152 34831052-4 2021 Furthermore, reactive oxygen species (ROS), act as an intermediate to activate NLRP3, contributing to subsequent inflammatory cascades and cell damage. Reactive Oxygen Species 38-41 NLR family pyrin domain containing 3 Homo sapiens 79-84 34625906-6 2022 The expression of NLRP3 inflammasome was detected after treatment with ROS scavenger. Reactive Oxygen Species 71-74 NLR family pyrin domain containing 3 Homo sapiens 18-23 34625906-11 2022 ROS scavenger inhibited the NLRP3 inflammatory response by inhibiting ROS levels. Reactive Oxygen Species 0-3 NLR family pyrin domain containing 3 Homo sapiens 28-33 34625906-11 2022 ROS scavenger inhibited the NLRP3 inflammatory response by inhibiting ROS levels. Reactive Oxygen Species 70-73 NLR family pyrin domain containing 3 Homo sapiens 28-33 34619679-6 2022 In THP-1 cells, beta-TCP increased also IL-18 production, and NLRP3 inflammasome activation by beta-TCP depended on phagocytosis, potassium efflux, and reactive oxygen species (ROS) generation. Reactive Oxygen Species 152-175 NLR family pyrin domain containing 3 Homo sapiens 62-67 34692754-0 2021 Attenuating Effect of Chlorella Extract on NLRP3 Inflammasome Activation by Mitochondrial Reactive Oxygen Species. Reactive Oxygen Species 90-113 NLR family pyrin domain containing 3 Homo sapiens 43-48 34619679-6 2022 In THP-1 cells, beta-TCP increased also IL-18 production, and NLRP3 inflammasome activation by beta-TCP depended on phagocytosis, potassium efflux, and reactive oxygen species (ROS) generation. Reactive Oxygen Species 177-180 NLR family pyrin domain containing 3 Homo sapiens 62-67 34616481-12 2021 Conclusion: The findings showed that XXMD could alleviate LPS-induced ALI injury and inhibit inflammation and suppress ROS/NLRP3 signaling pathway, which were involved in these protective effects. Reactive Oxygen Species 119-122 NLR family pyrin domain containing 3 Homo sapiens 123-128 34616481-9 2021 Results: Our results showed that XXMD attenuated LPS-induced oxidative stress, barrier dysfunction, and the activation of NLRP3 inflammasome in vitro, as evidenced by enhanced ROS production, TEER levels, expression of NLRP3 and caspase 1 (p20) and release of IL-1beta and IL-18, and weakened cell permeability. Reactive Oxygen Species 176-179 NLR family pyrin domain containing 3 Homo sapiens 122-127 34576117-6 2021 Further analysis using inhibitors of p38 MAPK, JNK, and NF-kappaB indicated that acute glucose shifts promoted IL-1beta secretion by activating the signaling pathway in a ROS-MAPK-NF-kappaB-NLRP3 inflammasome in THP-1 cells. Reactive Oxygen Species 171-174 NLR family pyrin domain containing 3 Homo sapiens 190-195 34262463-10 2021 Collectively, our results indicate that the ROS-NLRP3 inflammasome-interleukin-1beta axis may contribute to platelet hyperactivity in active CD. Reactive Oxygen Species 44-47 NLR family pyrin domain containing 3 Homo sapiens 48-53 34577552-1 2021 NLR family pyrin domain containing 3 (NLRP3) inflammasome formation is triggered by the damaged mitochondria releasing reactive oxygen species. Reactive Oxygen Species 119-142 NLR family pyrin domain containing 3 Homo sapiens 38-43 34147915-9 2021 We speculated that Cel relieves RA symptoms and inhibits inflammation by inhibiting the ROS-NF-kappaB-NLRP3 axis. Reactive Oxygen Species 88-91 NLR family pyrin domain containing 3 Homo sapiens 102-107 34577552-1 2021 NLR family pyrin domain containing 3 (NLRP3) inflammasome formation is triggered by the damaged mitochondria releasing reactive oxygen species. Reactive Oxygen Species 119-142 NLR family pyrin domain containing 3 Homo sapiens 0-36 34349888-2 2021 ROS induces NLRP3, a protein involved in the synthesis of interleukin (IL)-1 and IL-18; vaspin is a serine protease inhibitor that has an important role in suppressing the activation of NLRP3 inflammasome. Reactive Oxygen Species 0-3 NLR family pyrin domain containing 3 Homo sapiens 12-17 34202842-1 2021 NLRP3 inflammasome is a part of the innate immune system and responsible for the rapid identification and eradication of pathogenic microbes, metabolic stress products, reactive oxygen species, and other exogenous agents. Reactive Oxygen Species 169-192 NLR family pyrin domain containing 3 Homo sapiens 0-5 35136484-6 2022 In addition, upregulated PPARgamma inhibited the expression of the TXNIP/NLRP3 signaling pathway by reducing ROS-induced injury in the liver during sepsis, which further reduced NLRP3-mediated pyroptosis and the inflammatory response. Reactive Oxygen Species 109-112 NLR family pyrin domain containing 3 Homo sapiens 73-78 35403328-8 2022 Finally, the intracellular reactive oxygen species (ROS) was measured and the ROS inhibitor N-acetyl-L-cysteine (NAC) was used to investigate whether ROS was required for PM2.5-induced NLRP3 inflammasome activation and pyroptosis under ischemic conditions. Reactive Oxygen Species 150-153 NLR family pyrin domain containing 3 Homo sapiens 185-190 35403328-12 2022 Moreover, we observed that PM2.5 exposure increased the production of intracellular ROS following OGD/R, while inhibiting ROS production with NAC partially attenuated PM2.5-induced NLRP3 inflammasome activation and pyroptosis under ischemic conditions. Reactive Oxygen Species 84-87 NLR family pyrin domain containing 3 Homo sapiens 181-186 35403328-12 2022 Moreover, we observed that PM2.5 exposure increased the production of intracellular ROS following OGD/R, while inhibiting ROS production with NAC partially attenuated PM2.5-induced NLRP3 inflammasome activation and pyroptosis under ischemic conditions. Reactive Oxygen Species 122-125 NLR family pyrin domain containing 3 Homo sapiens 181-186 35403328-13 2022 CONCLUSION: These results suggested that PM2.5 exposure triggered the activation of NLRP3 inflammasome and pyroptosis under ischemic conditions, which may be mediated by increased ROS production after ischemic stroke. Reactive Oxygen Species 180-183 NLR family pyrin domain containing 3 Homo sapiens 84-89 35434015-5 2022 NLRP3 inflammasome activation was Reactive oxygen species (ROS) dependent, and the protein level was regulated when N-acetylcysteine (NAC) and adenosine triphosphate (ATP) were selected as tools for regulating ROS. Reactive Oxygen Species 34-57 NLR family pyrin domain containing 3 Homo sapiens 0-5 35434015-5 2022 NLRP3 inflammasome activation was Reactive oxygen species (ROS) dependent, and the protein level was regulated when N-acetylcysteine (NAC) and adenosine triphosphate (ATP) were selected as tools for regulating ROS. Reactive Oxygen Species 59-62 NLR family pyrin domain containing 3 Homo sapiens 0-5 35434015-5 2022 NLRP3 inflammasome activation was Reactive oxygen species (ROS) dependent, and the protein level was regulated when N-acetylcysteine (NAC) and adenosine triphosphate (ATP) were selected as tools for regulating ROS. Reactive Oxygen Species 210-213 NLR family pyrin domain containing 3 Homo sapiens 0-5 35434015-7 2022 NLRP3 inflammasome activation was sensitive to both ATP-mediated ROS level increases and NAC-mediated ROS inhibition, suggesting that ROS is associated with the activation of NLRP3 inflammasome in necroptosis. Reactive Oxygen Species 65-68 NLR family pyrin domain containing 3 Homo sapiens 0-5 35434015-7 2022 NLRP3 inflammasome activation was sensitive to both ATP-mediated ROS level increases and NAC-mediated ROS inhibition, suggesting that ROS is associated with the activation of NLRP3 inflammasome in necroptosis. Reactive Oxygen Species 102-105 NLR family pyrin domain containing 3 Homo sapiens 0-5 35434015-7 2022 NLRP3 inflammasome activation was sensitive to both ATP-mediated ROS level increases and NAC-mediated ROS inhibition, suggesting that ROS is associated with the activation of NLRP3 inflammasome in necroptosis. Reactive Oxygen Species 102-105 NLR family pyrin domain containing 3 Homo sapiens 175-180 35434015-7 2022 NLRP3 inflammasome activation was sensitive to both ATP-mediated ROS level increases and NAC-mediated ROS inhibition, suggesting that ROS is associated with the activation of NLRP3 inflammasome in necroptosis. Reactive Oxygen Species 134-137 NLR family pyrin domain containing 3 Homo sapiens 0-5 35434015-7 2022 NLRP3 inflammasome activation was sensitive to both ATP-mediated ROS level increases and NAC-mediated ROS inhibition, suggesting that ROS is associated with the activation of NLRP3 inflammasome in necroptosis. Reactive Oxygen Species 134-137 NLR family pyrin domain containing 3 Homo sapiens 175-180 35434015-9 2022 These results suggest that Nrf2 regulates NQO1 to attenuate ROS, which negatively regulates NLRP3 inflammasome. Reactive Oxygen Species 60-63 NLR family pyrin domain containing 3 Homo sapiens 92-97 35434015-10 2022 Conclusions: Nrf2/NQO1 was an inhibitor of ROS-induced NLRP3 inflammasome activation in Q-VD-OPH-induced necroptosis following cerebral I/R injury. Reactive Oxygen Species 43-46 NLR family pyrin domain containing 3 Homo sapiens 55-60 35634294-6 2022 Consistently, SHED could inhibit the elevated expression of NLRP3, GSDMD and Caspase-1 induced by CCl4 treatment in vitro co-culture system, which was mediated by decreasing reactive oxygen species (ROS) generation. Reactive Oxygen Species 199-202 NLR family pyrin domain containing 3 Homo sapiens 60-65 35490837-1 2022 We previously showed that increases in reactive oxygen species (ROS) generation upregulate NLRP3 inflammasome and inflammation through increases in both caspase-1 activity and rises in IL-1beta expression levels in animal models of dry eye (DE). Reactive Oxygen Species 39-62 NLR family pyrin domain containing 3 Homo sapiens 91-96 35490837-1 2022 We previously showed that increases in reactive oxygen species (ROS) generation upregulate NLRP3 inflammasome and inflammation through increases in both caspase-1 activity and rises in IL-1beta expression levels in animal models of dry eye (DE). Reactive Oxygen Species 64-67 NLR family pyrin domain containing 3 Homo sapiens 91-96 35394753-10 2022 The presence of mitochondrial reactive oxygen species (mitoROS) led to oxidative damage of mitochondrial DNA (mitoDNA), which further activates NLRP3/Caspase-1/gasdermin D (GSDMD)-dependent pyroptosis and could promote dendritic cell (DC) maturation by pyroptosis. Reactive Oxygen Species 30-53 NLR family pyrin domain containing 3 Homo sapiens 144-149 35437791-0 2022 ROS-mediated activation of NLRP3 inflammasome associated with pyroptosis in Het-1A cells induced by the co-exposure of nitrosamines. Reactive Oxygen Species 0-3 NLR family pyrin domain containing 3 Homo sapiens 27-32 35437791-6 2022 Pretreatment of reactive oxygen species scavenger N-acetyl-L-cysteine (NAC), particularly mitochondrial reactive oxygen species scavengers Mito-TEMPO, effectively inhibited the activation of NLRP3 inflammasome, suggesting that nitrosamines could mediate the activation of NLRP3 inflammasome via mitochondrial reactive oxygen species (mtROS). Reactive Oxygen Species 309-332 NLR family pyrin domain containing 3 Homo sapiens 191-196 34538111-4 2022 Recent Advances: Reactive oxygen species (ROS), especially derived from the mitochondria, are one of the critical mediators of NLRP3 inflammasome activation. Reactive Oxygen Species 17-40 NLR family pyrin domain containing 3 Homo sapiens 127-132 34538111-4 2022 Recent Advances: Reactive oxygen species (ROS), especially derived from the mitochondria, are one of the critical mediators of NLRP3 inflammasome activation. Reactive Oxygen Species 42-45 NLR family pyrin domain containing 3 Homo sapiens 127-132 34538111-5 2022 Furthermore, NLRP3 inflammasome-driven inflammation recruits inflammatory cells, including macrophages and neutrophils, which in turn cause ROS production, suggesting a feedback loop between ROS and NLRP3 inflammasome. Reactive Oxygen Species 140-143 NLR family pyrin domain containing 3 Homo sapiens 13-18 34538111-5 2022 Furthermore, NLRP3 inflammasome-driven inflammation recruits inflammatory cells, including macrophages and neutrophils, which in turn cause ROS production, suggesting a feedback loop between ROS and NLRP3 inflammasome. Reactive Oxygen Species 140-143 NLR family pyrin domain containing 3 Homo sapiens 199-204 34538111-5 2022 Furthermore, NLRP3 inflammasome-driven inflammation recruits inflammatory cells, including macrophages and neutrophils, which in turn cause ROS production, suggesting a feedback loop between ROS and NLRP3 inflammasome. Reactive Oxygen Species 191-194 NLR family pyrin domain containing 3 Homo sapiens 13-18 34538111-5 2022 Furthermore, NLRP3 inflammasome-driven inflammation recruits inflammatory cells, including macrophages and neutrophils, which in turn cause ROS production, suggesting a feedback loop between ROS and NLRP3 inflammasome. Reactive Oxygen Species 191-194 NLR family pyrin domain containing 3 Homo sapiens 199-204 34538111-6 2022 CRITICAL ISSUES: The precise mechanism of how ROS affects NLRP3 inflammasome activation still need to be addressed. Reactive Oxygen Species 46-49 NLR family pyrin domain containing 3 Homo sapiens 58-63 34538111-7 2022 This review will summarize the current knowledge on the molecular mechanisms underlying the activation of NLRP3 inflammasome with particular emphasis on the intricate balance of feedback loop between ROS and inflammasome activation. Reactive Oxygen Species 200-203 NLR family pyrin domain containing 3 Homo sapiens 106-111 35136484-6 2022 In addition, upregulated PPARgamma inhibited the expression of the TXNIP/NLRP3 signaling pathway by reducing ROS-induced injury in the liver during sepsis, which further reduced NLRP3-mediated pyroptosis and the inflammatory response. Reactive Oxygen Species 109-112 NLR family pyrin domain containing 3 Homo sapiens 178-183 34022434-5 2021 Mitochondrial dysfunction and subsequent accumulation of mitochondrial reactive oxygen species, mitochondrial deoxyribonucleic acid, and other mitochondria-associated proteins and lipids play vital roles in the instigation of the NLRP3 inflammasome. Reactive Oxygen Species 71-94 NLR family pyrin domain containing 3 Homo sapiens 230-235 35559886-6 2022 Metal ion, PAHs and surface ROS could also activate the NLRP3 inflammasome through mitochondrial ROS production. Reactive Oxygen Species 28-31 NLR family pyrin domain containing 3 Homo sapiens 56-61 35559886-6 2022 Metal ion, PAHs and surface ROS could also activate the NLRP3 inflammasome through mitochondrial ROS production. Reactive Oxygen Species 97-100 NLR family pyrin domain containing 3 Homo sapiens 56-61 35212954-2 2022 Specifically, mitochondrial dysfunction can induce NLRP3 inflammasome activation, where loss of mitochondrial potential leads to production of reactive oxygen species (ROS) and release of Ca2+, which in turn trigger inflammasome assembly. Reactive Oxygen Species 143-166 NLR family pyrin domain containing 3 Homo sapiens 51-56 35212954-2 2022 Specifically, mitochondrial dysfunction can induce NLRP3 inflammasome activation, where loss of mitochondrial potential leads to production of reactive oxygen species (ROS) and release of Ca2+, which in turn trigger inflammasome assembly. Reactive Oxygen Species 168-171 NLR family pyrin domain containing 3 Homo sapiens 51-56 33746978-7 2021 The suppression of the MSU-induced NLRP3 inflammasome activation is accompanied by the inhibition of lysosomal rupture, mitochondrial production of the reactive oxygen species (ROS), expression of cathepsins, and activity of cathepsin B, without affecting the crystal uptake and the expression of NLRP3 or pro-IL-1beta. Reactive Oxygen Species 152-175 NLR family pyrin domain containing 3 Homo sapiens 35-40 34054813-5 2021 Notably, excessive mitochondrial ROS (mtROS) was observed to trigger pyroptosis by activating the NLRP3 inflammasome, which was ameliorated by Mito-TEMPO treatment, indicating that the anti-pyroptotic role of PRX3 relies on its powerful ability to regulate mtROS. Reactive Oxygen Species 33-36 NLR family pyrin domain containing 3 Homo sapiens 98-103 33417223-6 2021 Intriguingly, blockade of ROS (Tempol) attenuated cocaine-mediated priming of NLRP3 and microglial activation (CD11b). Reactive Oxygen Species 26-29 NLR family pyrin domain containing 3 Homo sapiens 78-83 32893669-0 2021 Cpt1a promoted ROS-induced oxidative stress and inflammation in liver injury via the Nrf2/HO-1 and NLRP3 inflammasome signaling pathway. Reactive Oxygen Species 15-18 NLR family pyrin domain containing 3 Homo sapiens 99-104 32893669-6 2021 In summary, these data indicate that Cpt1a promotes ROS-induced oxidative stress in liver injury via the Nrf2/HO-1 and nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome signaling pathway. Reactive Oxygen Species 52-55 NLR family pyrin domain containing 3 Homo sapiens 119-184 32893669-6 2021 In summary, these data indicate that Cpt1a promotes ROS-induced oxidative stress in liver injury via the Nrf2/HO-1 and nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome signaling pathway. Reactive Oxygen Species 52-55 NLR family pyrin domain containing 3 Homo sapiens 186-191 33909257-7 2021 Mechanistically, bavachin specifically increases the production of nigericin-induced mitochondrial reactive oxygen species among the most important upstream events in the activation of the NLRP3 inflammasome. Reactive Oxygen Species 99-122 NLR family pyrin domain containing 3 Homo sapiens 189-194 33894359-5 2021 It also generates excessive Reactive oxygen species (ROS) and releases mtDNA into the cytoplasm, which causes induction of NLRP3 inflammasome and apoptosis. Reactive Oxygen Species 28-51 NLR family pyrin domain containing 3 Homo sapiens 123-128 33894359-5 2021 It also generates excessive Reactive oxygen species (ROS) and releases mtDNA into the cytoplasm, which causes induction of NLRP3 inflammasome and apoptosis. Reactive Oxygen Species 53-56 NLR family pyrin domain containing 3 Homo sapiens 123-128 32779379-0 2021 Exposure to environmental black carbon exacerbates nasal epithelial inflammation via the reactive oxygen species (ROS)-nucleotide-binding, oligomerization domain-like receptor family, pyrin domain containing 3 (NLRP3)-caspase-1-interleukin 1beta (IL-1beta) pathway. Reactive Oxygen Species 89-112 NLR family pyrin domain containing 3 Homo sapiens 211-216 32779379-0 2021 Exposure to environmental black carbon exacerbates nasal epithelial inflammation via the reactive oxygen species (ROS)-nucleotide-binding, oligomerization domain-like receptor family, pyrin domain containing 3 (NLRP3)-caspase-1-interleukin 1beta (IL-1beta) pathway. Reactive Oxygen Species 114-117 NLR family pyrin domain containing 3 Homo sapiens 211-216 32779379-10 2021 CONCLUSION: These findings suggest that exposure to BC and pollen can exaggerate oxidative stress and significantly increase the expression of IL-1beta in hNECs, and that this may involve a pathway integrating ROS-NLRP3-Caspase-1-IL-1beta signaling. Reactive Oxygen Species 210-213 NLR family pyrin domain containing 3 Homo sapiens 214-219 33746978-7 2021 The suppression of the MSU-induced NLRP3 inflammasome activation is accompanied by the inhibition of lysosomal rupture, mitochondrial production of the reactive oxygen species (ROS), expression of cathepsins, and activity of cathepsin B, without affecting the crystal uptake and the expression of NLRP3 or pro-IL-1beta. Reactive Oxygen Species 177-180 NLR family pyrin domain containing 3 Homo sapiens 35-40 33053467-5 2021 In addition, SiO2 NPs were found to promote the translocation and release of high-mobility group box 1 (HMGB1) from nucleus to cytoplasm, which was demonstrated to be regulated by ROS and NOD-like receptor pyrin domain containing 3 (NLRP3) inflammasome. Reactive Oxygen Species 180-183 NLR family pyrin domain containing 3 Homo sapiens 233-238 33630211-8 2021 In addition, Arg may regulate NLRP3 inflammasome activation partly through suppression of ROS production. Reactive Oxygen Species 90-93 NLR family pyrin domain containing 3 Homo sapiens 30-35 33630211-9 2021 In combination, we speculate that Arg exerts an inhibitory effect on the activation of NLRP3 inflammasome in ECs, which may be partly mediated by SIRT1 and ROS. Reactive Oxygen Species 156-159 NLR family pyrin domain containing 3 Homo sapiens 87-92 33626512-4 2021 Treating bone marrow-derived macrophages (BMDMs) with nicotine in vitro led to enhanced lipid phagocytosis, chemotaxis, and increased production of reactive oxygen species (ROS), which activated TXNIP/NLRP3 inflammasome signaling and promoted pyroptosis, as evidenced by caspase-1 cleavage and increased production of IL-1beta, IL-18, and gasdermin D. Reactive Oxygen Species 173-176 NLR family pyrin domain containing 3 Homo sapiens 201-206 33603947-7 2021 Therefore, P. acnes induces NPC pyroptosis via the ROS-NLRP3 signaling pathway, and the pyroptotic NPCs cause an IVD degeneration cascade. Reactive Oxygen Species 51-54 NLR family pyrin domain containing 3 Homo sapiens 55-60 33603947-0 2021 Propionibacterium acnes Accelerates Intervertebral Disc Degeneration by Inducing Pyroptosis of Nucleus Pulposus Cells via the ROS-NLRP3 Pathway. Reactive Oxygen Species 126-129 NLR family pyrin domain containing 3 Homo sapiens 130-135 33441928-2 2021 Inflammation in DE might be mediated by the NLRP3 inflammasome, which activated by exposure to reactive oxygen species (ROS). Reactive Oxygen Species 95-118 NLR family pyrin domain containing 3 Homo sapiens 44-49 33441928-2 2021 Inflammation in DE might be mediated by the NLRP3 inflammasome, which activated by exposure to reactive oxygen species (ROS). Reactive Oxygen Species 120-123 NLR family pyrin domain containing 3 Homo sapiens 44-49 33000581-10 2020 The mechanism could be that it reduced ROS produce and inhibited NLRP3 inflammasome activation so that mainly lower the downstream inflammatory cytokines IL-1beta and IL-18. Reactive Oxygen Species 39-42 NLR family pyrin domain containing 3 Homo sapiens 65-70 33292150-4 2020 Nlrp3 inflammasome elicit out an inflammatory response by emission of pro inflammatory cytokines by ROS (reactive oxygen species) production, mobilization of K+ efflux and Ca2+ and by activation of lysosome destabilization that eventually causes pyroptosis, a programmed cell death process. Reactive Oxygen Species 100-103 NLR family pyrin domain containing 3 Homo sapiens 0-5 33292150-4 2020 Nlrp3 inflammasome elicit out an inflammatory response by emission of pro inflammatory cytokines by ROS (reactive oxygen species) production, mobilization of K+ efflux and Ca2+ and by activation of lysosome destabilization that eventually causes pyroptosis, a programmed cell death process. Reactive Oxygen Species 105-128 NLR family pyrin domain containing 3 Homo sapiens 0-5 33011160-7 2020 Reactive oxygen species (ROS) scavengers, p38 and FOXO1 inhibitors and TXNIP siRNA inhibited TXNIP protein upregulation and NLRP3 inflammasome assembly and activation. Reactive Oxygen Species 0-23 NLR family pyrin domain containing 3 Homo sapiens 124-129 33011160-7 2020 Reactive oxygen species (ROS) scavengers, p38 and FOXO1 inhibitors and TXNIP siRNA inhibited TXNIP protein upregulation and NLRP3 inflammasome assembly and activation. Reactive Oxygen Species 25-28 NLR family pyrin domain containing 3 Homo sapiens 124-129 33011160-8 2020 Rosmarinic acid abrogated TXNIP protein upregulation and the interaction between TXNIP and NLRP3 to attenuate NLRP3 inflammasome assembly and activation and eventually IL-1beta secretion in ECs through downregulating ROS production, p38 phosphorylation and FOXO1 protein induction in ECs. Reactive Oxygen Species 217-220 NLR family pyrin domain containing 3 Homo sapiens 91-96 33011160-8 2020 Rosmarinic acid abrogated TXNIP protein upregulation and the interaction between TXNIP and NLRP3 to attenuate NLRP3 inflammasome assembly and activation and eventually IL-1beta secretion in ECs through downregulating ROS production, p38 phosphorylation and FOXO1 protein induction in ECs. Reactive Oxygen Species 217-220 NLR family pyrin domain containing 3 Homo sapiens 110-115 33131902-2 2020 Many triggers, including microbial pathogens (ie, bacteria and viruses) and other signals (ie, reactive oxygen species, adenosine triphosphate, urate, silicon, and asbestos), can stimulate the NLRP3 inflammasome. Reactive Oxygen Species 95-118 NLR family pyrin domain containing 3 Homo sapiens 193-198 33333846-6 2020 ROS play central roles in the activation of the NF-kappaB and NLRP3 signaling pathways via IkappaB (an inhibitor of NF-kappaB) and thioredoxin-interacting protein, respectively, thereby linking the molecular mechanisms of oxidative stress, inflammation and fibrosis. Reactive Oxygen Species 0-3 NLR family pyrin domain containing 3 Homo sapiens 62-67 32805375-7 2020 Using antioxidants to scavenge ROS and mtROS, we demonstrated that Nano-Co-induced mtROS generation was related to Nano-Co-induced NLRP3 inflammasome activation. Reactive Oxygen Species 31-34 NLR family pyrin domain containing 3 Homo sapiens 131-136 32805375-8 2020 Our findings demonstrated that Nano-Co exposure may promote intracellular oxidative stress damage, and mtROS may mediate the activation of the NLRP3 inflammasome in hepatocytes exposed to Nano-Co, suggesting an important role of ROS/NLRP3 pathway in Nano-Co-induced hepatotoxicity. Reactive Oxygen Species 105-108 NLR family pyrin domain containing 3 Homo sapiens 143-148 32805375-8 2020 Our findings demonstrated that Nano-Co exposure may promote intracellular oxidative stress damage, and mtROS may mediate the activation of the NLRP3 inflammasome in hepatocytes exposed to Nano-Co, suggesting an important role of ROS/NLRP3 pathway in Nano-Co-induced hepatotoxicity. Reactive Oxygen Species 105-108 NLR family pyrin domain containing 3 Homo sapiens 233-238 33324236-0 2020 Reactive Oxygen Species Interact With NLRP3 Inflammasomes and Are Involved in the Inflammation of Sepsis: From Mechanism to Treatment of Progression. Reactive Oxygen Species 0-23 NLR family pyrin domain containing 3 Homo sapiens 38-43 33324236-5 2020 Reactive oxygen species (ROS) are triggered by energy metabolism and respiratory dysfunction in sepsis, which not only cause oxidative damage to tissues and organelles, but also directly and indirectly promote NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome activation. Reactive Oxygen Species 0-23 NLR family pyrin domain containing 3 Homo sapiens 210-259 33324236-5 2020 Reactive oxygen species (ROS) are triggered by energy metabolism and respiratory dysfunction in sepsis, which not only cause oxidative damage to tissues and organelles, but also directly and indirectly promote NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome activation. Reactive Oxygen Species 0-23 NLR family pyrin domain containing 3 Homo sapiens 261-266 33324236-5 2020 Reactive oxygen species (ROS) are triggered by energy metabolism and respiratory dysfunction in sepsis, which not only cause oxidative damage to tissues and organelles, but also directly and indirectly promote NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome activation. Reactive Oxygen Species 25-28 NLR family pyrin domain containing 3 Homo sapiens 210-259 33324236-5 2020 Reactive oxygen species (ROS) are triggered by energy metabolism and respiratory dysfunction in sepsis, which not only cause oxidative damage to tissues and organelles, but also directly and indirectly promote NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasome activation. Reactive Oxygen Species 25-28 NLR family pyrin domain containing 3 Homo sapiens 261-266 32360740-0 2020 Insulin-like growth factor-I activates NFkappaB and NLRP3 inflammatory signalling via ROS in cancer cells. Reactive Oxygen Species 86-89 NLR family pyrin domain containing 3 Homo sapiens 52-57 32948742-6 2020 The danger signals for activating NLRP3 inflammasome are very extensive, especially reactive oxygen species (ROS), which act as an intermediate trigger to activate NLRP3 inflammasome, exacerbating subsequent inflammatory cascades and cell damage. Reactive Oxygen Species 84-107 NLR family pyrin domain containing 3 Homo sapiens 34-39 32948742-6 2020 The danger signals for activating NLRP3 inflammasome are very extensive, especially reactive oxygen species (ROS), which act as an intermediate trigger to activate NLRP3 inflammasome, exacerbating subsequent inflammatory cascades and cell damage. Reactive Oxygen Species 84-107 NLR family pyrin domain containing 3 Homo sapiens 164-169 32948742-6 2020 The danger signals for activating NLRP3 inflammasome are very extensive, especially reactive oxygen species (ROS), which act as an intermediate trigger to activate NLRP3 inflammasome, exacerbating subsequent inflammatory cascades and cell damage. Reactive Oxygen Species 109-112 NLR family pyrin domain containing 3 Homo sapiens 34-39 32948742-6 2020 The danger signals for activating NLRP3 inflammasome are very extensive, especially reactive oxygen species (ROS), which act as an intermediate trigger to activate NLRP3 inflammasome, exacerbating subsequent inflammatory cascades and cell damage. Reactive Oxygen Species 109-112 NLR family pyrin domain containing 3 Homo sapiens 164-169 32703754-4 2020 The activation of NLRP3 inflammasome is thought to be tightly associated with a regulator never in mitosis A (NIMA)-related kinase 7 (NEK7), apart from other signaling events such as K+ efflux and reactive oxygen species (ROS). Reactive Oxygen Species 197-220 NLR family pyrin domain containing 3 Homo sapiens 18-23 32703754-4 2020 The activation of NLRP3 inflammasome is thought to be tightly associated with a regulator never in mitosis A (NIMA)-related kinase 7 (NEK7), apart from other signaling events such as K+ efflux and reactive oxygen species (ROS). Reactive Oxygen Species 222-225 NLR family pyrin domain containing 3 Homo sapiens 18-23 32787872-13 2020 Ethanol-induced JNK1 phosphorylation activated the NLRP3 inflammasome that induced caspase-1 dependent mitophagy inhibition, thereby exacerbating ROS accumulation and causing cell death. Reactive Oxygen Species 146-149 NLR family pyrin domain containing 3 Homo sapiens 51-56 32966239-4 2020 Here, in an in vitro model for AS, we showed that NLRP3-depleted human aortic endothelial cells (HAECs) became resistant to apoptotic cell death, maintained proliferative potential and reduced reactive oxygen species (ROS) production upon treatment with oxidized low-density lipoprotein (ox-LDL). Reactive Oxygen Species 193-216 NLR family pyrin domain containing 3 Homo sapiens 50-55 32966239-4 2020 Here, in an in vitro model for AS, we showed that NLRP3-depleted human aortic endothelial cells (HAECs) became resistant to apoptotic cell death, maintained proliferative potential and reduced reactive oxygen species (ROS) production upon treatment with oxidized low-density lipoprotein (ox-LDL). Reactive Oxygen Species 218-221 NLR family pyrin domain containing 3 Homo sapiens 50-55 32574674-9 2020 More, CYP2J2 reduced LPS-induced reactive oxygen species (ROS) production and mitochondrial depolarization in heart cells, thereby inhibiting NLRP3 inflammasome activation. Reactive Oxygen Species 33-56 NLR family pyrin domain containing 3 Homo sapiens 142-147 32574674-9 2020 More, CYP2J2 reduced LPS-induced reactive oxygen species (ROS) production and mitochondrial depolarization in heart cells, thereby inhibiting NLRP3 inflammasome activation. Reactive Oxygen Species 58-61 NLR family pyrin domain containing 3 Homo sapiens 142-147 32360740-7 2020 Taken together, this is the first report on the mechanism by which IGF-1 activates NFkappaB and NLRP3 inflammatory signalling via ROS. Reactive Oxygen Species 130-133 NLR family pyrin domain containing 3 Homo sapiens 96-101 32334032-10 2020 Activation of the NLRP3 inflammasome was mediated by ROS, and ROS inhibitor treatment decreased the production of IL-1beta and IL-18 in vitro. Reactive Oxygen Species 53-56 NLR family pyrin domain containing 3 Homo sapiens 18-23 32592999-1 2020 Influenza virus M2 and PB1-F2 proteins have been proposed to activate the Nod-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome in macrophages by altering intracellular ionic balance or mitochondrial reactive oxygen species (ROS) production. Reactive Oxygen Species 219-242 NLR family pyrin domain containing 3 Homo sapiens 127-132 32592999-1 2020 Influenza virus M2 and PB1-F2 proteins have been proposed to activate the Nod-like receptor family, pyrin domain-containing 3 (NLRP3) inflammasome in macrophages by altering intracellular ionic balance or mitochondrial reactive oxygen species (ROS) production. Reactive Oxygen Species 244-247 NLR family pyrin domain containing 3 Homo sapiens 127-132 32334032-10 2020 Activation of the NLRP3 inflammasome was mediated by ROS, and ROS inhibitor treatment decreased the production of IL-1beta and IL-18 in vitro. Reactive Oxygen Species 62-65 NLR family pyrin domain containing 3 Homo sapiens 18-23 31612353-13 2020 Repression of ROS contributes to the inhibition of the expression of NLRP3, caspase-1 and IL-beta proteins as well as of cell migration. Reactive Oxygen Species 14-17 NLR family pyrin domain containing 3 Homo sapiens 69-74 32320383-7 2020 The results showed that ROS induced the pyroptosis of NPCs and it depended on the expression of NLRP3 and PYCARD. Reactive Oxygen Species 24-27 NLR family pyrin domain containing 3 Homo sapiens 96-101 31905258-11 2020 CONCLUSIONS: Cigarette smoke-induced pyroptosis of bladder tissue by activating ROS/NLRP3/caspase-1 signaling pathway. Reactive Oxygen Species 80-83 NLR family pyrin domain containing 3 Homo sapiens 84-89 31490096-0 2020 Plumbagin attenuated oxygen-glucose deprivation/reoxygenation-induced injury in human SH-SY5Y cells by inhibiting NOX4-derived ROS-activated NLRP3 inflammasome. Reactive Oxygen Species 127-130 NLR family pyrin domain containing 3 Homo sapiens 141-146 31490096-6 2020 Overall, PLB improved OGDR induced neuroinjury by inhibiting NOX4-derived ROS-activated NLRP3 inflammasome. Reactive Oxygen Species 74-77 NLR family pyrin domain containing 3 Homo sapiens 88-93 32508821-7 2020 NLRP3 inflammasome assembly is triggered by extracellular ATP, reactive oxygen species (ROS), potassium efflux, calcium misbalance, and lysosome disruption. Reactive Oxygen Species 63-86 NLR family pyrin domain containing 3 Homo sapiens 0-5 32508821-7 2020 NLRP3 inflammasome assembly is triggered by extracellular ATP, reactive oxygen species (ROS), potassium efflux, calcium misbalance, and lysosome disruption. Reactive Oxygen Species 88-91 NLR family pyrin domain containing 3 Homo sapiens 0-5 32156572-8 2020 Recent studies have reported that viroporin activity is capable of inducing inflammasome activity and production of IL-1beta, where NLRP3 is shown to be regulated by fluxes of K+, H+ and Ca2+ in addition to reactive oxygen species, autophagy and endoplasmic reticulum stress. Reactive Oxygen Species 207-230 NLR family pyrin domain containing 3 Homo sapiens 132-137 32320383-9 2020 In summary, ROS induces the pyroptosis of NPCs through the NLRP3/ PYCARD pathway, and establishes negative regulation by increasing autophagy and NFE2L2. Reactive Oxygen Species 12-15 NLR family pyrin domain containing 3 Homo sapiens 59-64 30860577-3 2019 Here, we also found MMP collapse and ROS generation induced by Nlrp3 inflammasome activation as previous studies reported. Reactive Oxygen Species 37-40 NLR family pyrin domain containing 3 Homo sapiens 63-68 31420721-7 2020 Also, it significantly suppresses the mitochondria-generated reactive oxygen species (ROS) required for NLRP3 inflammasome activation. Reactive Oxygen Species 61-84 NLR family pyrin domain containing 3 Homo sapiens 104-109 31420721-7 2020 Also, it significantly suppresses the mitochondria-generated reactive oxygen species (ROS) required for NLRP3 inflammasome activation. Reactive Oxygen Species 86-89 NLR family pyrin domain containing 3 Homo sapiens 104-109 30860577-8 2019 These results demonstrate that Gsdmd oxidation serves as a de novo mechanism by which mitochondrial ROS promote Nlrp3 inflammasome-dependent pyroptotic cell death. Reactive Oxygen Species 100-103 NLR family pyrin domain containing 3 Homo sapiens 112-117 31531346-1 2019 We previously demonstrated that angiotensin-(1-7) (Ang-(1-7)), an essential endocrine factor, inhibits the NLRP3 inflammasome by regulating reactive oxygen species (ROS) in fibrotic livers. Reactive Oxygen Species 140-163 NLR family pyrin domain containing 3 Homo sapiens 107-112 31694192-5 2019 Inflammasome-independent NLRP3 regulates apoptosis in tubular epithelial cells by interacting with mitochondria and mediating mitochondrial reactive oxygen species production and mitophagy. Reactive Oxygen Species 140-163 NLR family pyrin domain containing 3 Homo sapiens 25-30 31587010-0 2019 Advanced Glycation End Products (AGEs) Induce Apoptosis of Fibroblasts by Activation of NLRP3 Inflammasome via Reactive Oxygen Species (ROS) Signaling Pathway. Reactive Oxygen Species 111-134 NLR family pyrin domain containing 3 Homo sapiens 88-93 31587010-0 2019 Advanced Glycation End Products (AGEs) Induce Apoptosis of Fibroblasts by Activation of NLRP3 Inflammasome via Reactive Oxygen Species (ROS) Signaling Pathway. Reactive Oxygen Species 136-139 NLR family pyrin domain containing 3 Homo sapiens 88-93 31479495-7 2019 We also determined that MAYV triggers NLRP3 inflammasome activation by inducing reactive oxygen species (ROS) and potassium efflux. Reactive Oxygen Species 80-103 NLR family pyrin domain containing 3 Homo sapiens 38-43 31479495-7 2019 We also determined that MAYV triggers NLRP3 inflammasome activation by inducing reactive oxygen species (ROS) and potassium efflux. Reactive Oxygen Species 105-108 NLR family pyrin domain containing 3 Homo sapiens 38-43 31531346-0 2019 AVE 0991 Attenuates Pyroptosis and Liver Damage after Heatstroke by Inhibiting the ROS-NLRP3 Inflammatory Signalling Pathway. Reactive Oxygen Species 83-86 NLR family pyrin domain containing 3 Homo sapiens 87-92 31531346-1 2019 We previously demonstrated that angiotensin-(1-7) (Ang-(1-7)), an essential endocrine factor, inhibits the NLRP3 inflammasome by regulating reactive oxygen species (ROS) in fibrotic livers. Reactive Oxygen Species 165-168 NLR family pyrin domain containing 3 Homo sapiens 107-112 31531346-4 2019 We aimed to examine the change in angiotensin peptides in the livers affected by heatstroke and the effect on the ROS-NLRP3 inflammatory signalling pathway. Reactive Oxygen Species 114-117 NLR family pyrin domain containing 3 Homo sapiens 118-123 31531346-10 2019 In summary, AVE 0991 attenuates pyroptosis and liver damage induced by heat stress by inhibiting the ROS-NLRP3 inflammatory signalling pathway. Reactive Oxygen Species 101-104 NLR family pyrin domain containing 3 Homo sapiens 105-110 31311035-10 2019 After exposure of human ARPE-19 cells to excess atRAL, reactive oxygen species (ROS) (including mitochondrial ROS) and cathepsins released from lysosomes transmitted signals leading to NLRP3 inflammasome activation. Reactive Oxygen Species 55-78 NLR family pyrin domain containing 3 Homo sapiens 185-190 31265218-7 2019 XO-produced ROS also increase the synthesis of pro-IL-1beta, while the parasite activates caspase-1, providing the two necessary signals for the activation of the NLRP3 inflammasome. Reactive Oxygen Species 12-15 NLR family pyrin domain containing 3 Homo sapiens 163-168 31311035-10 2019 After exposure of human ARPE-19 cells to excess atRAL, reactive oxygen species (ROS) (including mitochondrial ROS) and cathepsins released from lysosomes transmitted signals leading to NLRP3 inflammasome activation. Reactive Oxygen Species 80-83 NLR family pyrin domain containing 3 Homo sapiens 185-190 31311035-10 2019 After exposure of human ARPE-19 cells to excess atRAL, reactive oxygen species (ROS) (including mitochondrial ROS) and cathepsins released from lysosomes transmitted signals leading to NLRP3 inflammasome activation. Reactive Oxygen Species 110-113 NLR family pyrin domain containing 3 Homo sapiens 185-190 31129032-0 2019 Corrigendum to "Reactive oxygen species promote tubular injury in diabetic nephropathy: The role of the mitochondrial ros-txnip-nlrp3 biological axis" [Redox Biology 16 (2018) 32-46]. Reactive Oxygen Species 16-39 NLR family pyrin domain containing 3 Homo sapiens 128-133 31129032-0 2019 Corrigendum to "Reactive oxygen species promote tubular injury in diabetic nephropathy: The role of the mitochondrial ros-txnip-nlrp3 biological axis" [Redox Biology 16 (2018) 32-46]. Reactive Oxygen Species 118-121 NLR family pyrin domain containing 3 Homo sapiens 128-133 30847537-9 2019 Induction of IL-1beta is dependent on the activation of the NLRP3 (NOD-like receptor family, pyrin domain containing 3) inflammasome and ROS (reactive oxygen species) production in macrophages, as inhibition of NLRP3 by MCC950 and reduction of ROS production by N-acetylcysteine blocked NLRP3 activation, IL-1beta induction, and fibroblast activation and differentiation. Reactive Oxygen Species 244-247 NLR family pyrin domain containing 3 Homo sapiens 60-65 30971058-6 2019 These data demonstrate that Asiatic acid both inhibits the activation of the NLRP3 inflammasome by downregulating mitochondrial reactive oxygen species directly to protect dopaminergic neurons from, and improves mitochondrial dysfunction in SH-SY5Y cells, which were established as a model of Parkinsons disease. Reactive Oxygen Species 128-151 NLR family pyrin domain containing 3 Homo sapiens 77-82 30246378-7 2019 In vivo, activation of NLRP3 inflammasomes with an increase of Ang-II type 1 receptor (AT1R) protein level and ROS production in human oral fibrosis tissues. Reactive Oxygen Species 111-114 NLR family pyrin domain containing 3 Homo sapiens 23-28 29887266-5 2019 Elevated production of reactive oxygen species could be able to activate NLRP3 inflammasome representing new deregulated biological machinery and a novel therapeutic target in hemodialysis patients. Reactive Oxygen Species 23-46 NLR family pyrin domain containing 3 Homo sapiens 73-78 30633869-7 2019 In addition, inhibition of estrogen receptor signaling or ROS production markedly blocked leptin-induced activation of NLRP3 inflammasomes, suggesting that estrogen receptor signaling and ROS production mediate inflammasomes activation by leptin. Reactive Oxygen Species 58-61 NLR family pyrin domain containing 3 Homo sapiens 119-124 30633869-7 2019 In addition, inhibition of estrogen receptor signaling or ROS production markedly blocked leptin-induced activation of NLRP3 inflammasomes, suggesting that estrogen receptor signaling and ROS production mediate inflammasomes activation by leptin. Reactive Oxygen Species 188-191 NLR family pyrin domain containing 3 Homo sapiens 119-124 29486589-1 2019 AIMS: The NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, which is activated by reactive oxygen species (ROS) and repressed by autophagy, has been identified as a novel agent of pulmonary fibrosis. Reactive Oxygen Species 105-128 NLR family pyrin domain containing 3 Homo sapiens 62-67 29486589-1 2019 AIMS: The NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, which is activated by reactive oxygen species (ROS) and repressed by autophagy, has been identified as a novel agent of pulmonary fibrosis. Reactive Oxygen Species 130-133 NLR family pyrin domain containing 3 Homo sapiens 62-67 29486589-12 2019 Innovation and Conclusion: Autophagy attenuates pulmonary fibrosis by regulating NLRP3 inflammasome activation induced by AngII-mediated ROS via redox balance modulation. Reactive Oxygen Species 137-140 NLR family pyrin domain containing 3 Homo sapiens 81-86 30761006-12 2019 CRP not only increased the expression of pro-IL-1beta and NLRP3 via the FcgammaRs/NF-kappaB pathway, but also promoted NLRP3 inflammasome activation and IL-1beta maturation by upregulation of reactive oxygen species (ROS) levels, purinergic receptor signaling, and activation of cysteine proteases. Reactive Oxygen Species 192-215 NLR family pyrin domain containing 3 Homo sapiens 119-124 30761006-12 2019 CRP not only increased the expression of pro-IL-1beta and NLRP3 via the FcgammaRs/NF-kappaB pathway, but also promoted NLRP3 inflammasome activation and IL-1beta maturation by upregulation of reactive oxygen species (ROS) levels, purinergic receptor signaling, and activation of cysteine proteases. Reactive Oxygen Species 217-220 NLR family pyrin domain containing 3 Homo sapiens 119-124 30761102-8 2019 K+ efflux and mitochondrial reactive oxygen species were important for SARS-CoV 3a-induced NLRP3 inflammasome activation. Reactive Oxygen Species 28-51 NLR family pyrin domain containing 3 Homo sapiens 91-96 30315709-0 2019 Role and mechanism of ROS scavengers in alleviating NLRP3-mediated inflammation. Reactive Oxygen Species 22-25 NLR family pyrin domain containing 3 Homo sapiens 52-57 30761138-12 2019 Inhibition of ROS by N-Acetyl Cysteine inhibited TLR2-induced priming of the NLRP3 inflammasome, but had no effect on MSU-induced activation. Reactive Oxygen Species 14-17 NLR family pyrin domain containing 3 Homo sapiens 77-82 30315709-3 2019 Recent evidence suggests the reactive oxygen species (ROS)-NLRP3 signaling pathway to be a possible NLRP3 inflammasome regulation model. Reactive Oxygen Species 29-52 NLR family pyrin domain containing 3 Homo sapiens 59-64 30315709-3 2019 Recent evidence suggests the reactive oxygen species (ROS)-NLRP3 signaling pathway to be a possible NLRP3 inflammasome regulation model. Reactive Oxygen Species 29-52 NLR family pyrin domain containing 3 Homo sapiens 100-105 30315709-3 2019 Recent evidence suggests the reactive oxygen species (ROS)-NLRP3 signaling pathway to be a possible NLRP3 inflammasome regulation model. Reactive Oxygen Species 54-57 NLR family pyrin domain containing 3 Homo sapiens 59-64 30315709-3 2019 Recent evidence suggests the reactive oxygen species (ROS)-NLRP3 signaling pathway to be a possible NLRP3 inflammasome regulation model. Reactive Oxygen Species 54-57 NLR family pyrin domain containing 3 Homo sapiens 100-105 30315709-5 2019 This article, at first, briefly overviews how ROS may mediate the regulation of NLRP3 inflammasome activation. Reactive Oxygen Species 46-49 NLR family pyrin domain containing 3 Homo sapiens 80-85 30315709-6 2019 Then, preclinical researches of various ROS scavengers for treating NLRP3 inflammasome-associated diseases are focused on and critically analyzed. Reactive Oxygen Species 40-43 NLR family pyrin domain containing 3 Homo sapiens 68-73 30389501-12 2019 In summary, we have demonstrated that SREBP-1 could be a key player in oxLDL-induced excessive lipid accumulation leading to macrophage FCF via ROS-mediated NLRP3/IL-1beta/SREBP-1 pathway. Reactive Oxygen Species 144-147 NLR family pyrin domain containing 3 Homo sapiens 157-162 30378427-1 2018 Our previous study showed that tetrachlorobenzoquinone (TCBQ) mediated the activation of Nod-like receptor protein 3 (NLRP3) inflammasome, which involves K+ efflux, reactive oxygen species (ROS) production, and mitochondrial DNA damage. Reactive Oxygen Species 165-188 NLR family pyrin domain containing 3 Homo sapiens 89-116 30471618-8 2019 We also found that ROS generation induced by high glucose-based PD solutions disrupts the TRX1-TXNIP association, while promoting the binding of TXNIP to NLRP3 in HPMCs. Reactive Oxygen Species 19-22 NLR family pyrin domain containing 3 Homo sapiens 154-159 30471618-9 2019 Furthermore, the application of a ROS inhibitor (APDC) to HPMCs blocked the high glucose-based PD solution-induced TXNIP-NLRP3 binding, in addition to ROS production and IL-1beta expression. Reactive Oxygen Species 34-37 NLR family pyrin domain containing 3 Homo sapiens 121-126 30378427-1 2018 Our previous study showed that tetrachlorobenzoquinone (TCBQ) mediated the activation of Nod-like receptor protein 3 (NLRP3) inflammasome, which involves K+ efflux, reactive oxygen species (ROS) production, and mitochondrial DNA damage. Reactive Oxygen Species 165-188 NLR family pyrin domain containing 3 Homo sapiens 118-123 30378427-1 2018 Our previous study showed that tetrachlorobenzoquinone (TCBQ) mediated the activation of Nod-like receptor protein 3 (NLRP3) inflammasome, which involves K+ efflux, reactive oxygen species (ROS) production, and mitochondrial DNA damage. Reactive Oxygen Species 190-193 NLR family pyrin domain containing 3 Homo sapiens 89-116 30378427-1 2018 Our previous study showed that tetrachlorobenzoquinone (TCBQ) mediated the activation of Nod-like receptor protein 3 (NLRP3) inflammasome, which involves K+ efflux, reactive oxygen species (ROS) production, and mitochondrial DNA damage. Reactive Oxygen Species 190-193 NLR family pyrin domain containing 3 Homo sapiens 118-123 30459926-5 2018 Although reactive oxygen species from mitochondria have been reported to be involved in the activation of the NLRP3 inflammasome in microglial cells upon the deposition of Abeta, whether Abeta directly or indirectly activates the NLRP3 inflammasome remains unclear. Reactive Oxygen Species 9-32 NLR family pyrin domain containing 3 Homo sapiens 110-115 29932955-3 2018 Reactive oxygen species (ROS) (in particular, mitochondrial ROS) contribute to NRLP3 activation via a well-elucidated mechanism involving oxidation of reduced thioredoxin and association of thioredoxin-interacting protein with NLRP3. Reactive Oxygen Species 0-23 NLR family pyrin domain containing 3 Homo sapiens 227-232 29932955-3 2018 Reactive oxygen species (ROS) (in particular, mitochondrial ROS) contribute to NRLP3 activation via a well-elucidated mechanism involving oxidation of reduced thioredoxin and association of thioredoxin-interacting protein with NLRP3. Reactive Oxygen Species 25-28 NLR family pyrin domain containing 3 Homo sapiens 227-232 29932955-3 2018 Reactive oxygen species (ROS) (in particular, mitochondrial ROS) contribute to NRLP3 activation via a well-elucidated mechanism involving oxidation of reduced thioredoxin and association of thioredoxin-interacting protein with NLRP3. Reactive Oxygen Species 60-63 NLR family pyrin domain containing 3 Homo sapiens 227-232 30422993-7 2018 It was noted that decreased NLRP3 inflammasome activation was associated with inhibited nuclear factor (NF)-kappaB activation, reduced reactive oxygen species production and increased autophagy. Reactive Oxygen Species 135-158 NLR family pyrin domain containing 3 Homo sapiens 28-33 30205151-6 2018 Moreover, the scavenging ROS relieved the autophagy, NLRP3 inflammasome activation and pyroptosis. Reactive Oxygen Species 25-28 NLR family pyrin domain containing 3 Homo sapiens 53-58 30307163-6 2018 We found that NLRP3 interference could inhibit HG-induced ROS. Reactive Oxygen Species 58-61 NLR family pyrin domain containing 3 Homo sapiens 14-19 30404007-0 2018 Shiga Toxin/Lipopolysaccharide Activates Caspase-4 and Gasdermin D to Trigger Mitochondrial Reactive Oxygen Species Upstream of the NLRP3 Inflammasome. Reactive Oxygen Species 92-115 NLR family pyrin domain containing 3 Homo sapiens 132-137 30404007-6 2018 Together, these data show that Stx2/LPS complex activates the non-canonical inflammasome and mitochondrial ROS upstream of the NLRP3 inflammasome to promote cytokine maturation and pyroptosis. Reactive Oxygen Species 107-110 NLR family pyrin domain containing 3 Homo sapiens 127-132 30307163-9 2018 Besides, TGFB1 induced the activation of NLRP3 inflammasome and the generation of ROS, which were blocked by NLRP3 interference or NAC. Reactive Oxygen Species 82-85 NLR family pyrin domain containing 3 Homo sapiens 109-114 30307163-11 2018 These results indicated that knockdown of NLRP3 antagonized HG-induced EMT by inhibiting ROS production, phosphorylation of SMAD3, P38MAPK and ERK1/2, highlighting NLRP3 as a potential therapy target for diabetic nephropathy. Reactive Oxygen Species 89-92 NLR family pyrin domain containing 3 Homo sapiens 42-47