The PINK1/Parkin signaling pathway-mediated mitophagy: a forgotten protagonist in myocardial ischemia/reperfusion injury
- PMID: 39419133
 - DOI: 10.1016/j.phrs.2024.107466
 
The PINK1/Parkin signaling pathway-mediated mitophagy: a forgotten protagonist in myocardial ischemia/reperfusion injury
Abstract
Myocardial ischemia causes extensive damage, further exacerbated by reperfusion, a phenomenon called myocardial ischemia/reperfusion injury (MIRI). Nowadays, the pathological mechanisms of MIRI have received extensive attention. Oxidative stress, multiple programmed cell deaths, inflammation and others are all essential pathological mechanisms contributing to MIRI. Mitochondria are the energy supply centers of cells. Numerous studies have found that abnormal mitochondrial function is an essential "culprit" of MIRI, and mitophagy mediated by the phosphatase and tensin homolog (PTEN)-induced kinase 1 (PINK1)/Parkin signaling pathway is an integral part of maintaining mitochondrial function. Therefore, exploring the association between the PINK1/Parkin signaling pathway-mediated mitophagy and MIRI is crucial. This review will mainly summarize the crucial role of the PINK1/Parkin signaling pathway-mediated mitophagy in MIR-induced several pathological mechanisms and various potential interventions that affect the PINK1/Parkin signaling pathway-mediated mitophagy, thus ameliorating MIRI.
Keywords: Dapagliflozin (PubChem CID: 9887712); Dexmedetomidine (PubChem CID: 5311068); Dexpramipexole (PubChem CID: 59868); Dl-3-n-butylphthalide (PubChem CID: 61361); Gastrodin (PubChem CID: 115067); Honokiol (PubChem CID: 72303); Intervention protocols; MIRI; Melatonin (PubChem CID: 896); Mitophagy; Pathological mechanisms; Potential interventions; Resveratrol (PubChem CID: 445154); Simvastatin (PubChem CID: 54454); Sitagliptin (PubChem CID: 4369359); The PINK1/Parkin signaling pathway.
Copyright © 2024 The Authors. Published by Elsevier Ltd.. All rights reserved.
Conflict of interest statement
Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
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