ArticleBurns & trauma2019
Tumor necrosis factor receptor-associated protein 1 regulates hypoxia-induced apoptosis through a mitochondria-dependent pathway mediated by cytochrome c oxidase subunit II.
Article in Burns & trauma, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Beyond Folding: Expanding the Functional Landscape of Hsp90 Chaperone Machinery in Health and Disease.International journal of molecular sciences · 2025Review
- Anti-oxidative-initiated cognitive impairment amelioration in Alzheimer's disease model rats through preventive transcutaneous electrical acupoint stimulation.Integrative medicine research · 2023Article
- The development of cancers research based on mitochondrial heat shock protein 90.Frontiers in oncology · 2023Review
- Melatonin as a regulator of apoptosis in leukaemia: molecular mechanism and therapeutic perspectives.Frontiers in pharmacology · 2023Review
- Using multi-tissue transcriptome-wide association study to identify candidate susceptibility genes for respiratory infectious diseases.Frontiers in genetics · 2023Article
- TRAP1 Chaperones the Metabolic Switch in Cancer.Biomolecules · 2022Review
- Hormetic effect of low doses of rapamycin triggers anti-aging cascades in WRL-68 cells by modulating an mTOR-mitochondria cross-talk.Molecular biology reports · 2022Article
- Overexpression of LncRNA MNX1-AS1/PPFIA4 Activates AKT/HIF-1Journal of oncology · 2022Article
- TRAP1 in Oxidative Stress and Neurodegeneration.Antioxidants (Basel, Switzerland) · 2021Review
- Exogenous L-carnitine ameliorates burn-induced cellular and mitochondrial injury of hepatocytes by restoring CPT1 activity.Nutrition & metabolism · 2021Article
- Ruscogenin attenuated tight junction injury and tumor migration in colorectal liver metastasis mice via regulating TRAP1.Translational cancer research · 2021Article
- The Mitochondrial Hsp90 TRAP1 and Alzheimer's Disease.Frontiers in molecular biosciences · 2021Review
- Effects of Neck-Arm Restraint Suspension of Beef Carcasses on Meat Quality and Proteome of Different Muscles During Post-mortem Aging.Frontiers in nutrition · 2021Article
- Old and New Approaches to Target the Hsp90 Chaperone.Current cancer drug targets · 2020Review
- Downregulation of TRAP1 aggravates injury of H9c2 cardiomyocytes in a hyperglycemic state.Experimental and therapeutic medicine · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundTumor necrosis factor receptor-associated protein 1 (TRAP1) plays a protective effect in hypoxic cardiomyocytes, but the precise mechanisms are not well clarified. The study is aimed to identify the mechanism of TRAP1 on hypoxic damage in cardiomyocytes.
methodsIn this study, the effects of TRAP1 and cytochrome c oxidase subunit II (COXII) on apoptosis in hypoxia-induced cardiomyocytes were explored using overexpression and knockdown methods separately.
resultsHypoxia induced cardiomyocyte apoptosis, and TRAP1 overexpression notably inhibited apoptosis induced by hypoxia. Conversely, TRAP1 silencing promoted apoptosis in hypoxic cardiomyocytes. Further investigation revealed that the proapoptotic effects caused by the silencing of TRAP1 were prevented by COXII overexpression, whereas COXII knockdown reduced the antiapoptotic function induced by TRAP1 overexpression. Additionally, changes in the release of cytochrome c from mitochondria into the cytosol and the caspase-3 activity in the cytoplasm, as well as reactive oxygen species production, were found to be correlated with the changes in apoptosis.
conclusionsThe current study uncovered that TRAP1 regulates hypoxia-induced cardiomyocyte apoptosis through a mitochondria-dependent apoptotic pathway mediated by COXII, in which reactive oxygen species presents as an important component.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.