PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 29033853-0 2017 Proinflammatory Effect of High Glucose Concentrations on HMrSV5 Cells via the Autocrine Effect of HMGB1. Glucose 31-38 high mobility group box 1 Homo sapiens 98-103 29033853-9 2017 Results: The major findings of these analyses were: (1) MCs secreted HMGB1 from the nucleus during exposure to high glucose levels; HMGB1 acted in an autocrine fashion on the MCs to promote the production of MCP-1 and IL-8; (2) HMGB1 had little effect on high-glucose-induced apoptosis of the MCs; and (3) HMGB1-mediated MCP-1 and IL-8 production depended on the activation of MAPK signaling pathways. Glucose 260-267 high mobility group box 1 Homo sapiens 132-137 29033853-5 2017 Aim: In this study, we aimed to explore the effect and underlying mechanism of endogenous HMGB1 in high-glucose-induced MC injury. Glucose 104-111 high mobility group box 1 Homo sapiens 90-95 29033853-9 2017 Results: The major findings of these analyses were: (1) MCs secreted HMGB1 from the nucleus during exposure to high glucose levels; HMGB1 acted in an autocrine fashion on the MCs to promote the production of MCP-1 and IL-8; (2) HMGB1 had little effect on high-glucose-induced apoptosis of the MCs; and (3) HMGB1-mediated MCP-1 and IL-8 production depended on the activation of MAPK signaling pathways. Glucose 260-267 high mobility group box 1 Homo sapiens 132-137 29033853-9 2017 Results: The major findings of these analyses were: (1) MCs secreted HMGB1 from the nucleus during exposure to high glucose levels; HMGB1 acted in an autocrine fashion on the MCs to promote the production of MCP-1 and IL-8; (2) HMGB1 had little effect on high-glucose-induced apoptosis of the MCs; and (3) HMGB1-mediated MCP-1 and IL-8 production depended on the activation of MAPK signaling pathways. Glucose 260-267 high mobility group box 1 Homo sapiens 132-137 29033853-9 2017 Results: The major findings of these analyses were: (1) MCs secreted HMGB1 from the nucleus during exposure to high glucose levels; HMGB1 acted in an autocrine fashion on the MCs to promote the production of MCP-1 and IL-8; (2) HMGB1 had little effect on high-glucose-induced apoptosis of the MCs; and (3) HMGB1-mediated MCP-1 and IL-8 production depended on the activation of MAPK signaling pathways. Glucose 116-123 high mobility group box 1 Homo sapiens 69-74 29033853-10 2017 In conclusion, endogenous HMGB1 plays an important role in the inflammatory reaction induced by high glucose on MCs via mitogen-activated protein kinase (MAPK) signaling pathways, but it seems to have little effect on high-glucose-induced apoptosis. Glucose 101-108 high mobility group box 1 Homo sapiens 26-31 28514198-6 2017 The current study further indicated that piceatannol decreased the expression of sbp-1 (encodes an ortholog of mammalian sterol regulatory element-binding protein) and its target gene fasn-1 (encodes an ortholog of fatty acid synthase) as well as increased the expression of hosl-1 (encodes an ortholog of hormone-sensitive lipase) in glucose-treated worms. Glucose 335-342 high mobility group box 1 Homo sapiens 81-86 26888251-9 2016 HMGB1 was significantly increased in RECs and Muller cells grown in high-glucose culture conditions, which was subsequently reduced with Compound 49b treatment. Glucose 73-80 high mobility group box 1 Homo sapiens 0-5 27560926-7 2017 High glucose induced a significant upregulation of HMGB1 and pSTAT-3 upregulation and nuclear translocation in retinal Muller cells. Glucose 5-12 high mobility group box 1 Homo sapiens 51-56 27560926-8 2017 GA co-treatment normalized the high-glucose-induced upregulation of HMGB1 and pSTAT-3 upregulation and nuclear translocation in Muller cells. Glucose 36-43 high mobility group box 1 Homo sapiens 68-73 26888251-10 2016 Our findings suggest that high glucose may increase HMGB1 levels that lead to increased TLR4 signaling. Glucose 31-38 high mobility group box 1 Homo sapiens 52-57 26845344-8 2016 The functional consequence of HMGB1 depletion in HCT116 and INS1 cells was reduced insulin and TCF7L2 mRNA expression, TCF7L2 transcriptional activity and glucose stimulated insulin secretion. Glucose 155-162 high mobility group box 1 Homo sapiens 30-35 25896065-9 2015 High-mobility group box-1 (HMGB-1), an endogenous activator of TLR4, rapidly increased in TLR4 immunoprecipitates upon high glucose stimulation, and this association was reduced by N-acetylcysteine, an antioxidant. Glucose 124-131 high mobility group box 1 Homo sapiens 0-25 26770371-0 2015 Effect of high mobility group box 1 on the human retinal pigment epithelial cell in high-glucose condition. Glucose 89-96 high mobility group box 1 Homo sapiens 10-35 26770371-6 2015 In the advanced in-vitro study, we detect the protective effect of HMGB1 on the RPE cells in high glucose condition. Glucose 98-105 high mobility group box 1 Homo sapiens 67-72 26770371-10 2015 Besides, HMGB1 treatment would up-regulate the expression of VEGFA in the RPE cells in high glucose condition. Glucose 92-99 high mobility group box 1 Homo sapiens 9-14 26454330-3 2015 This study explored HMGB-1 as a therapeutic target for DR treatment through observing its role in retinal ganglion cells (GRCs) in a high glucose environment. Glucose 138-145 high mobility group box 1 Homo sapiens 20-26 26454330-9 2015 RESULTS: HMGB-1 mRNA was up-regulated (P=0.015) and protein secretion increased (P=0.022) in the high glucose environment. Glucose 102-109 high mobility group box 1 Homo sapiens 9-15 26261550-0 2015 HMGB1 is activated in type 2 diabetes mellitus patients and in mesangial cells in response to high glucose. Glucose 99-106 high mobility group box 1 Homo sapiens 0-5 26261550-4 2015 In the present study, we examined the promotion by high glucose to High-mobility group box-1 (HMGB1) in patients with type 2 diabetes mellitus or in renal mesangial SV40 MES 13 cells. Glucose 56-63 high mobility group box 1 Homo sapiens 67-92 26261550-4 2015 In the present study, we examined the promotion by high glucose to High-mobility group box-1 (HMGB1) in patients with type 2 diabetes mellitus or in renal mesangial SV40 MES 13 cells. Glucose 56-63 high mobility group box 1 Homo sapiens 94-99 26261550-7 2015 The in vitro results indicated that HMGB1 mediated the D-glucose-induced pro-inflammatory cytokines in mesangial cells. Glucose 55-64 high mobility group box 1 Homo sapiens 36-41 26261550-9 2015 In summary, the present study indicated that HMGB1 was significantly promoted by the glucose in vivo or in vitro, in an association with an upregulation of pro-inflammatory cytokines, via activating NF-kappaB signaling pathway. Glucose 85-92 high mobility group box 1 Homo sapiens 45-50 26261550-10 2015 And the strategy of HMGB1 inhibition reduced the upregulation of pro-inflammatory cytokines in response to high glucose, via inhibiting the NF-kappaB signaling pathway. Glucose 112-119 high mobility group box 1 Homo sapiens 20-25 26131056-10 2015 Increased blood glucose levels may contribute to the increased HMGB1 levels. Glucose 16-23 high mobility group box 1 Homo sapiens 63-68 25896065-10 2015 An HMGB-1 inhibitor glycyrrhizin suppressed high glucose-induced Syk activation. Glucose 49-56 high mobility group box 1 Homo sapiens 3-9 25896065-12 2015 High glucose induces an immediate, reactive oxygen species-dependent, extracellular release of HMGB-1 which binds to TLR4 and activates it, leading to Syk activation. Glucose 5-12 high mobility group box 1 Homo sapiens 95-101 26948869-3 2016 HMGB1 allosterically inhibits the tetrameric pyruvate kinase isoform M2, thus blocking glucose-driven aerobic respiration. Glucose 87-94 high mobility group box 1 Homo sapiens 0-5 26760176-2 2016 OBJECTIVES: To verify high-mobility group box 1 protein (HMGB1) levels in CF patients according to glucose tolerance state, and analyze relationships with insulin secretion and resistance. Glucose 99-106 high mobility group box 1 Homo sapiens 22-47 26760176-2 2016 OBJECTIVES: To verify high-mobility group box 1 protein (HMGB1) levels in CF patients according to glucose tolerance state, and analyze relationships with insulin secretion and resistance. Glucose 99-106 high mobility group box 1 Homo sapiens 57-62 26131056-2 2015 This study was to investigate the relationship between average blood glucose level and HMGB1 level in CAD with T2DM patients. Glucose 69-76 high mobility group box 1 Homo sapiens 87-92 25896065-9 2015 High-mobility group box-1 (HMGB-1), an endogenous activator of TLR4, rapidly increased in TLR4 immunoprecipitates upon high glucose stimulation, and this association was reduced by N-acetylcysteine, an antioxidant. Glucose 124-131 high mobility group box 1 Homo sapiens 27-33 22862965-5 2012 The number of CD34-positive cells was negatively correlated with the serum levels of glucose and hemoglobin A1c, whereas the HMGB-1-positive area was positively correlated with the levels of serum glucose. Glucose 197-204 high mobility group box 1 Homo sapiens 125-131 25303153-6 2014 HMGB1 was increased in the supernatants of cells exposed to 30 mM and 11.2 mM glucose compared to control. Glucose 78-85 high mobility group box 1 Homo sapiens 0-5 24965297-1 2014 Intraperitoneal glucose degradation products (GDP) load influences systemic advanced glycation end products (AGEs) but the effects on soluble receptor for AGEs (s-RAGE) and its proinflammatory ligands: extracellular newly identified receptor for advanced glycation end-products binding protein(EN-RAGE) and high mobility group box-1 protein (HMGB-1) are unknown. Glucose 16-23 high mobility group box 1 Homo sapiens 307-332 24965297-1 2014 Intraperitoneal glucose degradation products (GDP) load influences systemic advanced glycation end products (AGEs) but the effects on soluble receptor for AGEs (s-RAGE) and its proinflammatory ligands: extracellular newly identified receptor for advanced glycation end-products binding protein(EN-RAGE) and high mobility group box-1 protein (HMGB-1) are unknown. Glucose 16-23 high mobility group box 1 Homo sapiens 342-348 24133029-8 2013 RESULTS: HMGB1 signalling pathway components including receptors for HMGB1 as well as NF-kappaB and TNFalpha/VEGF were significantly upregulated in type 2 diabetic retinas and in high glucose treated ARPE-19 cells, compared to their respective counterparts. Glucose 184-191 high mobility group box 1 Homo sapiens 9-14 24133029-9 2013 HMGB1 blockage significantly alleviated NF-kappaB activity and VEGF secretion in ARPE-19 cells cultured with high glucose. Glucose 114-121 high mobility group box 1 Homo sapiens 0-5 23576640-6 2013 Glucose (11.2 mM) maximally increased TLR2 and 4 expression, HMGB1 release, and NF-kappaB activation with increased expression of cytokines. Glucose 0-7 high mobility group box 1 Homo sapiens 61-66 23576640-10 2013 Therefore, short-term moderate increases in glucose in vitro increase HMGB1, which mediates NF-kappaB activation through both TLR2 and 4. Glucose 44-51 high mobility group box 1 Homo sapiens 70-75 23928875-0 2013 High mobility group box 1 (HMGB1) mediates high-glucose-induced calcification in vascular smooth muscle cells of saphenous veins. Glucose 48-55 high mobility group box 1 Homo sapiens 0-25 23928875-0 2013 High mobility group box 1 (HMGB1) mediates high-glucose-induced calcification in vascular smooth muscle cells of saphenous veins. Glucose 48-55 high mobility group box 1 Homo sapiens 27-32 23928875-4 2013 Therefore, the role of their common ligand, high mobility group box 1 (HMGB1), in high-glucose-induced calcification in VSMC of saphenous vein was investigated. Glucose 87-94 high mobility group box 1 Homo sapiens 44-69 23928875-4 2013 Therefore, the role of their common ligand, high mobility group box 1 (HMGB1), in high-glucose-induced calcification in VSMC of saphenous vein was investigated. Glucose 87-94 high mobility group box 1 Homo sapiens 71-76 23928875-6 2013 We first demonstrated high-glucose-induced HMGB1 translocation from nucleus to cytosol, and this translocation was induced through a NADPH oxidase and PKC-dependent pathway. Glucose 27-34 high mobility group box 1 Homo sapiens 43-48 23928875-8 2013 Then, we revealed downregulating HMGB1 expression abolished high-glucose-induced calcification accompanied by NFkappaB inactivation and low expression of bone morphogenetic protein-2 (BMP-2). Glucose 65-72 high mobility group box 1 Homo sapiens 33-38 23928875-11 2013 Our findings thus suggest HMGB1 plays an important role in mediating the calcification process induced by high glucose through NFkappaB activation and BMP-2 expression in VSMC of saphenous vein. Glucose 111-118 high mobility group box 1 Homo sapiens 26-31 23403945-0 2013 Insulin infusion suppresses while glucose infusion induces Toll-like receptors and high-mobility group-B1 protein expression in mononuclear cells of type 1 diabetes patients. Glucose 34-41 high mobility group box 1 Homo sapiens 83-105 23403945-4 2013 Glucose infusion led to an increase in plasma glucose concentration from 115 (fasting) to 215 (at 4 and 6 h) mg/dl and to an increase in ROS generation, the expression of TLR-4, TLR-2, TLR-1, HMGB1, p38 MAP kinase, and JNK-1, and plasma concentrations of HMGB1. Glucose 0-7 high mobility group box 1 Homo sapiens 192-197 23403945-4 2013 Glucose infusion led to an increase in plasma glucose concentration from 115 (fasting) to 215 (at 4 and 6 h) mg/dl and to an increase in ROS generation, the expression of TLR-4, TLR-2, TLR-1, HMGB1, p38 MAP kinase, and JNK-1, and plasma concentrations of HMGB1. Glucose 0-7 high mobility group box 1 Homo sapiens 255-260 32902022-0 2021 MiR-381-3p inhibits high glucose-induced vascular smooth muscle cell proliferation and migration by targeting HMGB1. Glucose 25-32 high mobility group box 1 Homo sapiens 110-115 19956840-2 2010 We have previously shown that metabolic stress due to glucose depletion (GD) induces necrosis and HMGB1 release through mitochondrial ROS production in A549 lung adenocarcinoma cells. Glucose 54-61 high mobility group box 1 Homo sapiens 98-103 18090368-10 2008 There was a significant correlation between CSF HMGB1 levels and CSF white blood cell counts and glucose levels in patients with bacterial meningitis. Glucose 97-104 high mobility group box 1 Homo sapiens 48-53 16641887-1 2006 Pyruvic acid, an intermediate metabolite of glucose, an effective scavenger of reactive oxygen species (ROS), inhibits tumor necrosis factor-alpha production and NF-kappaB signaling pathways, reduces circulating levels of HMGB1 (high mobility group B1), decreases COX-2 (cyclo-oxygenase-2), iNOS (inducible nitric oxide synthase), and IL-6 (interleukin-6) mRNA expression in liver, ileal mucosa, and colonic mucosa in animal models with endotoxemia. Glucose 44-51 high mobility group box 1 Homo sapiens 222-227 16641887-1 2006 Pyruvic acid, an intermediate metabolite of glucose, an effective scavenger of reactive oxygen species (ROS), inhibits tumor necrosis factor-alpha production and NF-kappaB signaling pathways, reduces circulating levels of HMGB1 (high mobility group B1), decreases COX-2 (cyclo-oxygenase-2), iNOS (inducible nitric oxide synthase), and IL-6 (interleukin-6) mRNA expression in liver, ileal mucosa, and colonic mucosa in animal models with endotoxemia. Glucose 44-51 high mobility group box 1 Homo sapiens 229-251 34657898-7 2022 Correlation analysis indicated that the levels of HMGB1 and TLR4 were positively correlated with triglyceride (TG), fasting plasma glucose (FPG) levels and BMI, whereas a negative correlation between HMGB1 and high density lipoprotein (HDL) was noted. Glucose 131-138 high mobility group box 1 Homo sapiens 50-55 34639171-8 2021 Cardiomyocytes exposed to 25mM glucose resulted in the downregulation of HSP60 and SIRT1 after 48 h. We further examined that hyperglycemia mediated the decrease in the gap junction protein CX43, as well as CXC chemokine receptor CXCR4 which may affect the physiological functions of the cardiomyocytes when exposed to high glucose for 24 and 48 h. Upregulated expression of DNA-binding nuclear protein HMGB1, along with changes in histone methylation marker H3K9me1 have demonstrated hyperglycemia-induced damage to cardiomyocyte at 24 h of exposure. Glucose 31-38 high mobility group box 1 Homo sapiens 403-408 34639171-8 2021 Cardiomyocytes exposed to 25mM glucose resulted in the downregulation of HSP60 and SIRT1 after 48 h. We further examined that hyperglycemia mediated the decrease in the gap junction protein CX43, as well as CXC chemokine receptor CXCR4 which may affect the physiological functions of the cardiomyocytes when exposed to high glucose for 24 and 48 h. Upregulated expression of DNA-binding nuclear protein HMGB1, along with changes in histone methylation marker H3K9me1 have demonstrated hyperglycemia-induced damage to cardiomyocyte at 24 h of exposure. Glucose 324-331 high mobility group box 1 Homo sapiens 403-408 33565572-0 2021 HMGB1 regulates ferroptosis through Nrf2 pathway in mesangial cells in response to high glucose. Glucose 88-95 high mobility group box 1 Homo sapiens 0-5 33565572-2 2021 The present study explored the role of high-mobility group box-1 (HMGB1) on the regulation of ferroptosis in mesangial cells in response to high glucose. Glucose 145-152 high mobility group box 1 Homo sapiens 39-64 33565572-2 2021 The present study explored the role of high-mobility group box-1 (HMGB1) on the regulation of ferroptosis in mesangial cells in response to high glucose. Glucose 145-152 high mobility group box 1 Homo sapiens 66-71 33565572-6 2021 Furthermore, nuclear factor E2-related factor 2 (Nrf2) was decreased in DN patients and high glucose mediated translocation of HMGB1 in mesangial cells. Glucose 93-100 high mobility group box 1 Homo sapiens 127-132 33565572-7 2021 Knockdown of HMGB1 suppressed high glucose-induced activation of TLR4/NF-kappaB axis and promoted Nrf2 expression as well as its downstream targets including HO-1, NQO-1, GCLC and GCLM. Glucose 35-42 high mobility group box 1 Homo sapiens 13-18 33565572-8 2021 Collectively, these findings suggest that HMGB1 regulates glucose-induced ferroptosis via Nrf2 pathway in mesangial cells. Glucose 58-65 high mobility group box 1 Homo sapiens 42-47 20514411-5 2010 We observed that CuZnSOD and MnSOD overexpression prevents metabolic stress-induced necrosis and HMGB1 release by inhibiting mitochondrial ROS and intracellular O2- production in response to glucose depletion in two dimensional cell culture. Glucose 191-198 high mobility group box 1 Homo sapiens 97-102 32902022-13 2021 CONCLUSION: MiR-381-3p targets HMGB1 to suppress the inflammation, oxidative stress, proliferation and migration of high-glucose-induced VSMCs by targeting HMGB1. Glucose 121-128 high mobility group box 1 Homo sapiens 31-36 32902022-13 2021 CONCLUSION: MiR-381-3p targets HMGB1 to suppress the inflammation, oxidative stress, proliferation and migration of high-glucose-induced VSMCs by targeting HMGB1. Glucose 121-128 high mobility group box 1 Homo sapiens 156-161 32469087-7 2020 Concurrently, HMGB1 impaired insulin sensitivities by attenuating the abundance of insulin receptor substrate-1, Akt phosphorylation, GLUT4 translocation, and glucose uptake in granulosa cells, which were reversed by blocking autophagy pathways with siRNA-mediated knockdown of ATG7 or with chloroquine and bafilomycin A1, the lysosome inhibitors. Glucose 159-166 high mobility group box 1 Homo sapiens 14-19 32497617-2 2020 HMGB1 is a danger associated protein pattern receptor which can sense high glucose as a stressor. Glucose 75-82 high mobility group box 1 Homo sapiens 0-5 30871870-4 2019 In NCM460 cells, under the normal glucose state, proliferation increased by overexpression of HMGB1. Glucose 34-41 high mobility group box 1 Homo sapiens 94-99 31353785-2 2019 HMGB1 is implicated in hyperglycemia and excess glucose in trophoblast. Glucose 48-55 high mobility group box 1 Homo sapiens 0-5 32208365-8 2020 In addition, mimic-induced miR-142-3p elevation resulted in decreased HMGB1 and LC3II levels and elevated p62 levels in the high-glucose condition, whereas miR-142-3p knockdown had the reverse effects, and metformin abolished those effects. Glucose 129-136 high mobility group box 1 Homo sapiens 70-75 32208365-9 2020 Metformin inhibits high glucose-induced VSMC hyperproliferation and increased migration by inducing miR-142-3p-mediated inhibition of HMGB1 expression via the HMGB1-autophagy related pathway. Glucose 24-31 high mobility group box 1 Homo sapiens 134-139 32208365-9 2020 Metformin inhibits high glucose-induced VSMC hyperproliferation and increased migration by inducing miR-142-3p-mediated inhibition of HMGB1 expression via the HMGB1-autophagy related pathway. Glucose 24-31 high mobility group box 1 Homo sapiens 159-164 31087368-3 2019 Here, we reported that high mobility group box 1 (HMGB1) was highly elevated in high glucose (HG)-treated mesangial cells, and induced the phosphorylation, nuclear translocation, and DNA binding activity of NF-kappaB via toll-like receptor 4 (TLR4). Glucose 85-92 high mobility group box 1 Homo sapiens 23-48 31087368-3 2019 Here, we reported that high mobility group box 1 (HMGB1) was highly elevated in high glucose (HG)-treated mesangial cells, and induced the phosphorylation, nuclear translocation, and DNA binding activity of NF-kappaB via toll-like receptor 4 (TLR4). Glucose 85-92 high mobility group box 1 Homo sapiens 50-55 31351069-7 2019 We also show that orexin A inhibits high glucose-induced expression of TxNIP, which is crucial to the activation of the NLRP3 inflammasome, as well as that of HMGB1. Glucose 41-48 high mobility group box 1 Homo sapiens 159-164 31298304-11 2019 RESULTS: In the presence of high glucose, hRECs cells proliferation was significantly reduced, Caspase-3 activity was enhanced, LDH and ROS levels were increased, SOD activity was declined with increased expression of HMGB-1, NF-kappaB, VEGF, as well as secretion of TNF-alpha and IL-1beta compared with control group (p < 0.05). Glucose 33-40 high mobility group box 1 Homo sapiens 218-224 30871870-5 2019 Under a high glucose state, increased expression of HMGB1 was accompanied with a release from cell nuclei into the cytoplasm and extracellular matrix. Glucose 13-20 high mobility group box 1 Homo sapiens 52-57 30055307-9 2018 However, HMGB1 overexpression attenuated the protective effect of miR-106 on HUVECs in high glucose conditions. Glucose 92-99 high mobility group box 1 Homo sapiens 9-14 30328477-0 2018 PKA regulates HMGB1 through activation of IGFBP-3 and SIRT1 in human retinal endothelial cells cultured in high glucose. Glucose 112-119 high mobility group box 1 Homo sapiens 14-19 30328477-11 2018 High glucose inhibited SIRT1 levels and increased cytoplasmic HMGB1 in REC. Glucose 5-12 high mobility group box 1 Homo sapiens 62-67 30055307-5 2018 The results showed that the expression of HMGB1 was increased in human umbilical vein endothelial cells (HUVECs) after exposure to high glucose (25 mM). Glucose 136-143 high mobility group box 1 Homo sapiens 42-47 30055307-6 2018 Downregulation of HMGB1 attenuated the high glucose-induced antiangiogenesis of HUVECs, and the decrease expression of HMGB1 inhibiting HUVEC apoptosis and inflammatory factor expression. Glucose 44-51 high mobility group box 1 Homo sapiens 18-23 30055307-12 2018 Taken together, these data collectively suggested that miR-106 was a potential molecular target for inhibiting high glucose-induced inflammation and apoptosis by targeting HMGB1. Glucose 116-123 high mobility group box 1 Homo sapiens 172-177 30175447-0 2018 Excess glucose induce trophoblast inflammation and limit cell migration through HMGB1 activation of Toll-Like receptor 4. Glucose 7-14 high mobility group box 1 Homo sapiens 80-85 30175447-10 2018 RESULTS: Excess glucose triggered a trophoblast sterile inflammatory IL-8 and antimigratory response through HMGB1 activation of TLR4. Glucose 16-23 high mobility group box 1 Homo sapiens 109-114 30119194-13 2018 The inhibition of HMGB1 by glycyrrhizin also confirmed the involvement of HMGB1/TLR4/NF-kappaB/NLRP3 pathway in high glucose-induced SH-SY5Y cells. Glucose 117-124 high mobility group box 1 Homo sapiens 18-23 30119194-13 2018 The inhibition of HMGB1 by glycyrrhizin also confirmed the involvement of HMGB1/TLR4/NF-kappaB/NLRP3 pathway in high glucose-induced SH-SY5Y cells. Glucose 117-124 high mobility group box 1 Homo sapiens 74-79 30081847-0 2018 Intermittent high glucose-induced oxidative stress modulates retinal pigmented epithelial cell autophagy and promotes cell survival via increased HMGB1. Glucose 18-25 high mobility group box 1 Homo sapiens 146-151 29704473-8 2018 With regard to cardiovascular risk, levels of serum HMGB1 were positively associated with 10-year CHD risk (beta coefficient 0.506, 95% CI 0.030 to 0.983, p = .037), independent of patients" undiagnosed abnormal glucose regulation. Glucose 212-219 high mobility group box 1 Homo sapiens 52-57