PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 28377599-4 2017 On the contrary, ozone (abundant component of air NTP) treatment alone, exhibited the highest levels of reactive oxygen species production leading to CypD-related necrosis via the mitochondrial permeability transition. Reactive Oxygen Species 104-127 peptidylprolyl isomerase D Homo sapiens 150-154 33309700-8 2021 In the matrix these peptides, which would fold into alpha-helical structure in native conditions, interact with cyclophilin D (CypD) and upon stimulation by elevated ROS and/or the Ca2+ spontaneously misfold into beta-sheet ion conducting pores, causing PTP opening. Reactive Oxygen Species 166-169 peptidylprolyl isomerase D Homo sapiens 127-131 29541521-5 2018 Our data demonstrate that high dose laser irradiation exhibited the highest levels of total reactive oxygen species production, leading to cyclophilin D-related necrosis via the mitochondrial permeability transition. Reactive Oxygen Species 92-115 peptidylprolyl isomerase D Homo sapiens 139-152 28273124-8 2017 And the protective effects of blocking CypD in Dex-induced gingival fibroblasts dysfunction were evidenced by rescued mitochondrial function and suppressed production of reactive oxygen species (ROS). Reactive Oxygen Species 170-193 peptidylprolyl isomerase D Homo sapiens 39-43 28273124-8 2017 And the protective effects of blocking CypD in Dex-induced gingival fibroblasts dysfunction were evidenced by rescued mitochondrial function and suppressed production of reactive oxygen species (ROS). Reactive Oxygen Species 195-198 peptidylprolyl isomerase D Homo sapiens 39-43 28273124-9 2017 In addition, blockade of CypD by pharmaceutical inhibitor CsA or gene knockdown also restored Dex-induced cell toxicity in HGF-1 cells, as shown by suppressed mitochondrial ROS production, increased CcO activity and decreased apoptosis. Reactive Oxygen Species 173-176 peptidylprolyl isomerase D Homo sapiens 25-29 23382999-7 2013 The potential mechanisms of the protective effects of lacking CypD on Abeta-induced abnormal mitochondrial transport in axon are increased axonal calcium buffer capability, diminished reactive oxygen species (ROS), and suppressing downstream signal transduction P38 activation. Reactive Oxygen Species 209-212 peptidylprolyl isomerase D Homo sapiens 62-66 28351946-0 2017 Stress-induced dynamic regulation of mitochondrial STAT3 and its association with cyclophilin D reduce mitochondrial ROS production. Reactive Oxygen Species 117-120 peptidylprolyl isomerase D Homo sapiens 82-95 28351946-8 2017 Binding of STAT3 to CypD was mediated by the amino terminus of STAT3, which was also important for reducing mitochondrial ROS production after oxidative stress. Reactive Oxygen Species 122-125 peptidylprolyl isomerase D Homo sapiens 20-24 23195208-0 2012 Cyclophilin D: a therapeutic target to counteract reactive oxygen species-mediated damage in neurodegenerative disease? Reactive Oxygen Species 50-73 peptidylprolyl isomerase D Homo sapiens 0-13