Mechanism of mitochondrial autophagy in myocardial ischemia-reperfusion injury

Abstract

Abstract:

Cardiovascular disease is still one of the most common causes of death in the world. In the past, timely reperfusion treatment has greatly reduced the death rate of the disease while promoting blood recovery and cardiomyocyte recovery. Ischemia reperfusion (IR) injury is an inevitable pathological process in many clinical practices. The mechanisms of myocardial IR injury include a variety of pathological processes such as mitochondrial autophagy and apoptosis, and these signaling pathways are interrelated and act on each other. Among them, mitochondrial autophagy has attracted wide attention as a selective autophagy. Mitochondrial autophagy maintains the normal operation of cardiomyocytes by regulating the quality and quantity of mitochondria. However, as stimulated by oxidative stress, ischemia and hypoxia, excessive mitochondrial autophagy or insufficient mitochondrial autophagy can affect the function of cardiomyocytes and even lead to the death of cardiomyocytes. Therefore, the activation degree of mitochondrial autophagy in cardiomyocytes should be strictly controlled. This article reviews the mechanism and progress of mitochondrial autophagy in myocardial IR injury, aiming to provide some assistance in the study of myocardial IR injury.

Key words:Autophagy,Mitochondrial autophagy,Ischemia reperfusion injury

CLC Number:

R542.2

GAO Yue, XING Shifeng. Mechanism of mitochondrial autophagy in myocardial ischemia-reperfusion injury[J]. Journal of Internal Medicine Concepts & Practice, 2024, 19(05): 328-332.

References35

[1]	Giacomello M, Pyakurel A, Glytsou C, et al. The cell biology of mitochondrial membrane dynamics[J].Nat Rev Mol Cell Biol,2020,21(4):204-224.
[2]	Marzetti E, Calvani R, Landi F, et al. Mitochondrial quality control processes at the crossroads of cell death and survival: mechanisms and signaling pathways[J].Int J Mol Sci,2024,25(13):7305.
[3]	Nakatogawa H. Mechanisms governing autophagosome biogenesis[J].Nat Rev Mol Cell Biol,2020,21(8):439-458.
[4]	Gatica D, Lahiri V, Klionsky DJ. Cargo recognition and degradation by selective autophagy[J].Nat Cell Biol,2018,20(3):233-242. doi:10.1038/s41556-018-0037-zpmid:29476151
[5]	He J, Liu D, Zhao L, et al. Myocardial ischemia/reperfusion injury: mechanisms of injury and implications for management (Review)[J].Exp Ther Med,2022,23(6):430. doi:10.3892/etm.2022.11357pmid:35607376
[6]	张小赏, 童随阳, 操传斌. 紫苏醛对大鼠心肌缺血/再灌注损伤诱导的自噬的影响[J].湖北医药学院学报,2022,41(03):224-228.
[7]	De Duve C, Pressman BC, Gianetto R, et al. Tissue fractionation studies. 6. Intracellular distribution patterns of enzymes in rat-liver tissue[J].Biochem J,1955,60(4):604-617.
[8]	Rasool S, Veyron S, Soya N, et al. Mechanism of PINK1 activation by autophosphorylation and insights into assembly on the TOM complex[J].Mol Cell,2022,82(1):44-59.e6.
[9]	Vranas M, Lu Y, Rasool S, et al. Selective localization of Mfn2 near PINK1 enables its preferential ubiquitination by Parkin on mitochondria[J].Open Biol,2022,12(1):210255.
[10]	Tu M, Tan VP, Yu JD, et al. RhoA signaling increases mitophagy and protects cardiomyocytes against ischemia by stabilizing PINK1 protein and recruiting Parkin to mitochondria[J].Cell Death Differ,2022,29(12):2472-2486. doi:10.1038/s41418-022-01032-wpmid:35760846
[11]	Wang M, Wan C, He T, et al. Sigma-1 receptor regulates mitophagy in dopaminergic neurons and contributes to dopaminergic protection[J].Neuropharmacology,2021,196:108360.
[12]	Qi MM, Sun RM, Wang QY, et al. Astragalosideivimproved oxidative stress induced injury through pink1/parkin-mediated mitophagy in h9c2 cells[J].J Hypertens Suppl,2023,41 Suppl 3:e253.
[13]	Xia N, Strand S, Schlufter F, et al. Role of SIRT1 and FOXO factors in eNOS transcriptional activation by resveratrol[J].Nitric Oxide,2013,32:29-35. doi:10.1016/j.niox.2013.04.001pmid:23583951
[14]	Yi C, Tong J, Lu P, et al. Formation of a Snf1-Mec1-Atg1 module on mitochondria governs energy deprivation-induced autophagy by regulating mitochondrial respiration[J].Dev Cell,2017,41(1):59-71. doi:S1534-5807(17)30160-0pmid:28399401
[15]	张贵君, 汪瑶, 李军令, 等. 电针对帕金森病小鼠SIRT3/PINK1/Parkin通路介导的线粒体自噬的影响[J].针刺研究,2024,49(03):221-230.
[16]	Guan S, Xin Y, Ding Y, et al. Ginsenoside Rg1 protects against cardiac remodeling in heart failure via SIRT1/PINK1/Parkin-mediated mitophagy[J].Chem Biodivers,2023,20(2):e202200730.
[17]	Li S, Zhang J, Liu C, et al. The role of mitophagy in regulating cell death[J].Oxid Med Cell Longev,2021,2021:6617256.
[18]	胡丽君, 魏燕, 贺行巍, 等. 过表达双特异性蛋白磷酸酶1通过调节自噬作用减轻阿霉素诱导的心肌细胞凋亡和心肌纤维化[J].岭南心血管病杂志,2023,29(02):190-197.
[19]	Rahman M, Nguyen TM, Lee GJ, et al. Unraveling the role of ras homolog enriched in brain (rheb1 and rheb2): bridging neuronal dynamics and cancer pathogenesis through mechanistic target of rapamycin signaling[J].Int J Mol Sci,2024,25(3):1489.
[20]	赵辉.基于PI3K-AKT-mTORC1信号通路研究参地颗粒对慢性肾炎患者及MsPGN大鼠线粒体自噬的调节作用[D]. 安徽中医药大学,2020.
[21]	Zhang T, Xue L, Li L, et al. BNIP3 protein suppresses PINK1 kinase proteolytic cleavage to promote mitophagy[J].J Biol Chem,2016,291(41):21616-21629. pmid:27528605
[22]	Li A, Gao M, Liu B, et al. Mitochondrial autophagy: molecular mechanisms and implications for cardiovascular disease[J].Cell Death Dis,2022,13(5):444. doi:10.1038/s41419-022-04906-6pmid:35534453
[23]	Gok MO, Connor OM, Wang X, et al. The outer mitochondrial membrane protein TMEM11 demarcates spatially restricted BNIP3/BNIP3L-mediated mitophagy[J].J Cell Biol,2023,222(4):e202204021.
[24]	Yang L, Xie P, Wu J, et al. Deferoxamine treatment combined with sevoflurane postconditioning attenuates myocardial ischemia-reperfusion injury by restoring HIF-1/BNIP3-mediated mitochondrial autophagy in GK rats[J].Front Pharmacol,2020,11:6. doi:10.3389/fphar.2020.00006pmid:32140105
[25]	Zhang W. The mitophagy receptor FUN14 domain-containing 1 (FUNDC1): a promising biomarker and potential therapeutic target of human diseases[J].Genes Dis,2020,8(5):640-654.
[26]	Zhou H, Zhu P, Guo J, et al. Ripk3 induces mitochondrial apoptosis via inhibition of FUNDC1 mitophagy in cardiac IR injury[J].Redox Biol,2017,13:498-507. doi:S2213-2317(17)30425-1pmid:28732308
[27]	Turkieh A, El Masri Y, Pinet F, et al. Mitophagy regulation following myocardial infarction[J].Cells,2022,11(2):199.
[28]	Titus AS, Sung EA, Zablocki D, et al. Mitophagy for cardioprotection[J].Basic Res Cardiol,2023,118(1):42. doi:10.1007/s00395-023-01009-xpmid:37798455
[29]	Tan N, Liu T, Wang X, et al. The multi-faced role of FUNDC1 in mitochondrial events and human diseases[J].Front Cell Dev Biol,2022,10:918943.
[30]	Bragoszewski P, Turek M, Chacinska A. Control of mitochondrial biogenesis and function by the ubiquitin-proteasome system[J].Open Biol,2017,7(4):170007.
[31]	Mao Y, Ren J, Yang L. FUN14 domain containing 1 (FUNDC1): a promising mitophagy receptor regulating mitochondrial homeostasis in cardiovascular diseases[J].Front Pharmacol,2022,13:887045.
[32]	Choubey V, Zeb A, Kaasik A. Molecular mechanisms and regulation of mammalian mitophagy[J].Cells,2021,11(1):38.
[33]	Varela YR, González-Ramírez EJ, Iriondo MN, et al. Lipids in mitochondrial macroautophagy: phase behavior of bilayers containing cardiolipin and ceramide[J].Int J Mol Sci,2023,24(6):5080.
[34]	Pilátová MB, Solárová Z, Mezencev R, et al. Ceramides and their roles in programmed cell death[J].Adv Med Sci,2023,68(2):417-425.
[35]	Sheridan M, Ogretmen B. The role of ceramide metabolism and signaling in the regulation of mitophagy and cancer therapy[J].Cancers (Basel),2021,13(10):2475.