ArticleJournal of cellular and molecular medicine2019
Poly (ADP-ribose) polymerase inhibition protects against myocardial ischaemia/reperfusion injury via suppressing mitophagy.
Article in Journal of cellular and molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- Mitochondrial oxidative stress, calcium and dynamics in cardiac ischaemia-reperfusion injury.The Journal of physiology · 2026Review
- Ginsenoside Rg1 Alleviates Hydrogen Peroxide-Induced Autophagy and Apoptosis in Ovarian Granulosa Cells.Cell biochemistry and biophysics · 2025Article
- NADCells · 2025Review
- Review
- Mitochondria and myocardial ischemia/reperfusion injury: Effects of Chinese herbal medicine and the underlying mechanisms.Journal of pharmaceutical analysis · 2025Review
- Mitochondrial quality control in human health and disease.Military Medical Research · 2024Review
- Potential relationship between autophagy and ferroptosis in myocardial ischemia/reperfusion injury.Genes & diseases · 2023Review
- Regulation of autophagy of the heart in ischemia and reperfusion.Apoptosis : an international journal on programmed cell death · 2023Review
- Mitochondrial quality control in cardiac ischemia/reperfusion injury: new insights into mechanisms and implications.Cell biology and toxicology · 2023Review
- Relationship between ferroptosis and mitophagy in cardiac ischemia reperfusion injury: a mini-review.PeerJ · 2023Review
- Hydrogen therapy after resuscitation improves myocardial injury involving inhibition of autophagy in an asphyxial rat model of cardiac arrest.Experimental and therapeutic medicine · 2022Article
- The inhibition of PGAM5 suppresses seizures in a kainate-induced epilepsy modelFrontiers in molecular neuroscience · 2022Article
- Article
- Advances in Cardiotoxicity Induced by Altered Mitochondrial Dynamics and Mitophagy.Frontiers in cardiovascular medicine · 2021Review
- Melatonin Attenuates Anoxia/Reoxygenation Injury by Inhibiting Excessive Mitophagy Through the MT2/SIRT3/FoxO3a Signaling Pathway in H9c2 Cells.Drug design, development and therapy · 2020Article
- Poly (ADP-ribose) polymerase inhibition protects against myocardial ischaemia/reperfusion injury via suppressing mitophagy.Journal of cellular and molecular medicine · 2019Article
- Poly(ADP-Ribosyl) Code Functions.Acta naturaeArticle
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myocardial ischaemia/reperfusion (I/R) injury attenuates the beneficial effects of reperfusion therapy. Poly(ADP-ribose) polymerase (PARP) is overactivated during myocardial I/R injury. Mitophagy plays a critical role in the development of myocardial I/R injury. However, the effect of PARP activation on mitophagy in cardiomyocytes is unknown. In this study, we found that I/R induced PARP activation and mitophagy in mouse hearts. Poly(ADP-ribose) polymerase inhibition reduced the infarct size and suppressed mitophagy after myocardial I/R injury. In vitro, hypoxia/reoxygenation (H/R) activated PARP, promoted mitophagy and induced cell apoptosis in cardiomyocytes. Poly(ADP-ribose) polymerase inhibition suppressed H/R-induced mitophagy and cell apoptosis. Parkin knockdown with lentivirus vectors inhibited mitophagy and prevented cell apoptosis in H/R-treated cells. Poly(ADP-ribose) polymerase inhibition prevented the loss of the mitochondrial membrane potential (ΔΨm). Cyclosporin A maintained ΔΨm and suppressed mitophagy but FCCP reduced the effect of PARP inhibition on ΔΨm and promoted mitophagy, indicating the critical role of ΔΨm in H/R-induced mitophagy. Furthermore, reactive oxygen species (ROS) and poly(ADP-ribosylation) of CypD and TSPO might contribute to the regulation of ΔΨm by PARP. Our findings thus suggest that PARP inhibition protects against I/R-induced cell apoptosis by suppressing excessive mitophagy via the ΔΨm/Parkin pathway.
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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.