Research progress and function of mitophagy in myocardial infarction

ZHANG Wen-jing; LI Xiao-feng; SUN Ming-ming; PENG Hu

doi:10.16766/j.cnki.issn.1674-4152.002556

Volume 20 Issue 7

Jul. 2022

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Article Navigation > Chinese Journal of General Practice > 2022 > 20(7): 1194-1198

ZHANG Wen-jing, LI Xiao-feng, SUN Ming-ming, PENG Hu. Research progress and function of mitophagy in myocardial infarction[J]. Chinese Journal of General Practice, 2022, 20(7): 1194-1198. doi: 10.16766/j.cnki.issn.1674-4152.002556

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ZHANG Wen-jing, LI Xiao-feng, SUN Ming-ming, PENG Hu. Research progress and function of mitophagy in myocardial infarction[J]. Chinese Journal of General Practice, 2022, 20(7): 1194-1198. doi: 10.16766/j.cnki.issn.1674-4152.002556

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Research progress and function of mitophagy in myocardial infarction

doi: 10.16766/j.cnki.issn.1674-4152.002556

ZHANG Wen-jing^{1, 2}
, LI Xiao-feng²
, SUN Ming-ming²
, PENG Hu^{1, 2
,
,}

1.
Shanghai Tenth People's Hospital, School of Clinical Medicine, Nanjing Medical University, Shanghai 200072, China

Funds:

82000274

Received Date: 2022-02-08
Available Online: 2022-09-23

Abstract

Abstract

Myocardial infarction (MI) refers to myocardial ischemic necrosis caused by persistent and severe acute ischemia and hypoxia caused by acute reduction or interruption of perfusion blood flow after the coronary artery that nourishes the heart. The mechanism of myocardial injury in patients with MI needs to be clarified urgently. The research on the mechanism of MI and the search for intervention targets have important clinical value. The mitochondria, as organelles that provide energy, is the key organelles for the continuous contraction and relaxation of cardiac muscle cells. They are responsible for adenosine triphosphate generation and energy metabolism. The loss of mitochondrial integrity and function is a key pathological factor that changes the structure and function of the heart. Mitochondrial dysfunction during MI is an important mechanism of myocardial injury. Mitochondrial quality control refers to maintaining a balance between mitochondrial production and clearance, which is particularly essential for maintaining cell survival and function. Mitophagy is associated with various diseases, such as neurodegenerative diseases, cardiovascular diseases and cancer. Mitophagy is a selective autophagy that uses damaged mitochondria as an autophagy substrate to maintain cardiovascular homeostasis. Mitophagy controls the quality of the mitochondria by promoting the degradation and recycling of damaged mitochondria and protects cardiomyocytes from ischemic injury. For normal cardiomyocytes, sufficient mitochondrial production could ensure sufficient energy supply. However, in the process of MI, mitochondrial damage occurs in cardiomyocytes and if the damaged mitochondria are not cleared in time, cardiomyocyte damage and even apoptosis could be induced. The process of mitophagy is complex, involving many physiological and pathological processes, and it is regulated by various substances, such as proteins and RNAs. In this article, the important roles and related mechanisms of mitophagy in MI are reviewed.
- Mitophagy,
- Myocardial ischemic injury,
- Myocardial infarction

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References(47)

References

[1]	BENJAMIN E J, BLAHA M J, CHIUVE S E, et al. Heart disease and stroke statistics-2017 update: A report from the american heart association[J]. Circulation, 2017, 135(10): e146-e603.
[2]	茅焕豪, 叶剑飞, 郑伟峰, 等. 左西孟旦联合冻干重组人脑利钠肽对缺血性心肌病患者心室重构改善作用的研究[J]. 中华全科医学, 2021, 19(11): 1861-1863, 1950. doi: 10.16766/j.cnki.issn.1674-4152.002186 MAO H H, YE J F, ZHENG W F, et al. Effect of levosimendan combined with lyophilized recombinant human brain natriuretic peptide on ventricular remodeling in patients with ischemic cardiomyopathy[J]. Chinese J Gen Pract, 2021, 19(11): 1861-1863, 1950. doi: 10.16766/j.cnki.issn.1674-4152.002186
[3]	BAUTERS C, DUBOIS E, POROUCHANI S, et al. Long-term prognostic impact of left ventricular remodeling after a first myocardial infarction in modern clinical practice[J]. PLoS One, 2017, 12(11): e0188884. DOI: 10.1371/journal.pone.0188884.
[4]	SUN M M, ZHANG W J, BI Y G, et al. NDP52 protects against myocardial infarction-provoked cardiac anomalies through promoting autophagosome-lysosome fusion via recruiting TBK1 and RAB7[J]. Antioxid Redox Signal, 2021. DOI: 10.1089/ars.2020.8253.
[5]	BUGGER H, PFEIL K. Mitochondrial ROS in myocardial ischemia reperfusion and remodeling[J]. Biochim Biophys Acta Mol Basis Dis, 2020, 1866(7): 165768. DOI: 10.1016/j.bbadis.2020.165768.
[6]	ZHANG Y, JIAO L, SUN L H, et al. LncRNA ZFAS1 as a SERCA2a inhibitor to cause intracellular Ca²⁺ overload and contractile dysfunction in a mouse model of myocardial infarction[J]. Circ Res, 2018, 122(10): 1354-1368. doi: 10.1161/CIRCRESAHA.117.312117
[7]	SUI X B, LIANG X, CHEN L X, et al. Bacterial xenophagy and its possible role in cancer: A potential antimicrobial strategy for cancer prevention and treatment[J]. Autophagy, 2017, 13(2): 237-247. doi: 10.1080/15548627.2016.1252890
[8]	MANCIAS J D, KIMMELMAN A C. Mechanisms of selective autophagy in normal physiology and cancer[J]. J Mol Biol, 2016, 428(9 Pt A): 1659-1680.
[9]	ZHANG Y M, WHALEY-CONNELL A T, SOWERS J R, et al. Autophagy as an emerging target in cardiorenal metabolic disease: From pathophysiology to management[J]. Pharmacol Ther, 2018. DOI: 10.1016/j.pharmthera.2018.06.004.
[10]	ZHOU H, WANG S Y, HU S Y, et al. ER-Mitochondria microdomains in cardiac ischemia-reperfusion injury: A fresh perspective[J]. Front Physiol, 2018. DOI: 10.3389/fphys.2018.00755.
[11]	JI C H, KWON Y T. Crosstalk and interplay between the ubiquitin-proteasome system and autophagy[J]. Mol Cells, 2017, 40(7): 441-449.
[12]	XU C L, CAO Y P, LIU R X, et al. Mitophagy-regulated mitochondrial health strongly protects the heart against cardiac dysfunction after acute myocardial infarction[J]. J Cell Mol Med, 2022, 26(4): 1315-1326. doi: 10.1111/jcmm.17190
[13]	QIU F, YUAN Y, LUO W, et al. Asiatic acid alleviates ischemic myocardial injury in mice by modulating mitophagy- and glycophagy-based energy metabolism[J]. Acta Pharmacol Sin, 2021. DOI: 10.1038/s41401-021-00763-9.
[14]	ZHANG W L, CHEN C Y, WANG J, et al. Mitophagy in cardiomyocytes and in platelets: A major mechanism of cardioprotection against Ischemia/Reperfusion injury[J]. Physiology(Bethesda), 2018, 33(2): 86-98.
[15]	YANG M J, LINN B S, ZHANG Y M, et al. Mitophagy and mitochondrial integrity in cardiac ischemia-reperfusion injury[J]. Biochim Biophys Acta Mol Basis Dis, 2019, 1865(9): 2293-2302. doi: 10.1016/j.bbadis.2019.05.007
[16]	SEKINE S, YOULE R J. PINK1 import regulation; a fine system to convey mitochondrial stress to the cytosol[J]. BMC Biol, 2018, 16(1): 2. doi: 10.1186/s12915-017-0470-7
[17]	XIONG W J, HUA J H, LIU Z H, et al. PTEN induced putative kinase 1(PINK1)alleviates angiotensin Ⅱ-induced cardiac injury by ameliorating mitochondrial dysfunction[J]. Int J Cardiol, 2018. DOI: 10.1016/j.ijcard.2018.03.054.
[18]	ZHANG R H, KRIGMAN J, LUO H K, et al. Mitophagy in cardiovascular homeostasis[J]. Mech Ageing Dev, 2020. DOI: 10.1016/j.mad.2020.111245.
[19]	MORALES P E, ARIAS-DURÁN C, ÁVALOS-GUAJARDO Y, et al. Emerging role of mitophagy in cardiovascular physiology and pathology[J]. Mol Aspects Med, 2020. DOI: 10.1016/j.mam.2019.09.006.
[20]	LUO H K, ZHANG R H, KRIGMAN J, et al. A healthy heart and a healthy brain: Looking at mitophagy[J]. Front Cell Dev Biol, 2020. DOI: 10.3389/fcell.2020.00294.
[21]	WANG B, NIE J L, WU L J, et al. AMPKα2 protects against the development of heart failure by enhancing mitophagy via PINK1 phosphorylation[J]. Circ Res, 2018, 122(5): 712-729. doi: 10.1161/CIRCRESAHA.117.312317
[22]	XIN T, LU C Z. Irisin activates Opa1-induced mitophagy to protect cardiomyocytes against apoptosis following myocardial infarction[J]. Aging(Albany NY), 2020, 12(5): 4474-4488.
[23]	FENG Y S, ZHAO J, HOU H F, et al. WDR26 promotes mitophagy of cardiomyocytes induced by hypoxia through Parkin translocation[J]. Acta Biochim Biophys Sin(Shanghai), 2016, 48(12): 1075-1084.
[24]	JI W Q, WEI S J, HAO P P, et al. Aldehyde dehydrogenase 2 has cardioprotective effects on myocardial Ischaemia/Reperfusion injury via suppressing mitophagy[J]. Front Pharmacol, 2016. DOI: 10.3389/fphar.2016.00101.
[25]	ZHOU H, ZHANG Y, HU S Y, et al. Melatonin protects cardiac microvasculature against ischemia/reperfusion injury via suppression of mitochondrial fission-VDAC1-HK2-mPTP-mitophagy axis[J]. J Pineal Res, 2017. DOI: 10.1111/jpi.12413.
[26]	WU J J, YANG Y L, GAO Y F, et al. Melatonin attenuates Anoxia/Reoxygenation injury by inhibiting excessive mitophagy through the MT2/SIRT3/FoxO3a signaling pathway in H9c2 cells[J]. Drug Des Devel Ther, 2020. DOI: 10.2147/DDDT.S248628.
[27]	WU S N, LU Q L, WANG Q L, et al. Binding of FUN14 Domain Containing 1 with inositol 1, 4, 5-trisphosphate receptor in mitochondria-associated endoplasmic reticulum membranes maintains mitochondrial dynamics and function in hearts in vivo[J]. Circulation, 2017, 136(23): 2248-2266. doi: 10.1161/CIRCULATIONAHA.117.030235
[28]	CHEN G, HAN Z, FENG D, et al. A regulatory signaling loop comprising the PGAM5 phosphatase and CK2 controls receptor-mediated mitophagy[J]. Molecular Cell, 2014, 54(3): 362-377. doi: 10.1016/j.molcel.2014.02.034
[29]	LU W, SUN J H, YOON J S, et al. Mitochondrial protein PGAM5 regulates mitophagic protection against cell necroptosis[J]. PLoS One, 2016. DOI: 10.1371/journal.pone.0147792.
[30]	YU W C, XU M, ZHANG T, et al. Mst1 promotes cardiac ischemia-reperfusion injury by inhibiting the ERK-CREB pathway and repressing FUNDC1-mediated mitophagy[J]. J Physiol Sci, 2019, 69(1): 113-127. doi: 10.1007/s12576-018-0627-3
[31]	ZHANG W L, SIRAJ S, ZHANG R, et al. Mitophagy receptor FUNDC1 regulates mitochondrial homeostasis and protects the heart from I/R injury[J]. Autophagy, 2017, 13(6): 1080-1081. doi: 10.1080/15548627.2017.1300224
[32]	ZHOU H, LI D D, ZHU P J, et al. Melatonin suppresses platelet activation and function against cardiac ischemia/reperfusion injury via PPARγ/FUNDC1/mitophagy pathways[J]. J Pineal Res, 2017. DOI: 10.1111/jpi.12438.
[33]	JIN Q H, LI R B, HU N, et al. DUSP1 alleviates cardiac ischemia/reperfusion injury by suppressing the Mff-required mitochondrial fission and Bnip3-related mitophagy via the JNK pathways[J]. Redox Biol, 2018. DOI: 10.1016/j.redox.2017.11.004.
[34]	LEE T L, LEE M H, CHEN Y C, et al. Vitamin D attenuates Ischemia/Reperfusion-induced cardiac injury by reducing mitochondrial fission and mitophagy[J]. Front Pharmacol, 2020. DOI: 10.3389/fphar.2020.604700.
[35]	WHANG M I, TAVARES R M, BENJAMIN D I, et al. The ubiquitin binding protein TAX1BP1 mediates autophagasome induction and the metabolic transition of activated T cells[J]. Immunity, 2017, 46(3): 405-420. doi: 10.1016/j.immuni.2017.02.018
[36]	WANG Y, HAN Z H, XU Z J, et al. Protective effect of optic atrophy 1 on cardiomyocyte oxidative stress: roles of mitophagy, mitochondrial fission, and MAPK/ERK signaling[J]. Oxid Med Cell Longev, 2021. DOI: 10.1155/2021/3726885.
[37]	HOSHINO A, MITA Y, OKAWA Y, et al. Cytosolic p53 inhibits Parkin-mediated mitophagy and promotes mitochondrial dysfunction in the mouse heart[J]. Nat Commun, 2013. DOI: 10.1038/ncomms3308.
[38]	TAHRIR F, KNEZEVIC T, GUPTA M, et al. Evidence for the role of BAG3 in mitochondrial quality control in cardiomyocytes[J]. J Cell Physiol, 2017, 232(4): 797-805. doi: 10.1002/jcp.25476
[39]	TAHRIR F G, KNEZEVIC T, GUPTA M K, et al. Evidence for the role of BAG3 in mitochondrial quality control in cardiomyocytes[J]. J Cell Physiol, 2017, 232(4): 797-805. doi: 10.1002/jcp.25476
[40]	TURKIEH A, CHARRIER H, DUBOIS-DERUY E, et al. Noncoding RNAs in cardiac autophagy following myocardial infarction[J]. Oxid Med Cell Longev, 2019. DOI: 10.1155/2019/8438650.
[41]	WANG L N, LI Q, DIAO J Y, et al. MiR-23a is involved in myocardial Ischemia/Reperfusion injury by directly targeting CX43 and regulating mitophagy[J]. Inflammation, 2021, 44(4): 1581-1591. doi: 10.1007/s10753-021-01443-w
[42]	WANG S H, ZHU X L, WANG F, et al. LncRNA H19 governs mitophagy and restores mitochondrial respiration in the heart through Pink1/Parkin signaling during obesity[J]. Cell Death Dis, 2021, 12(6): 557. doi: 10.1038/s41419-021-03821-6
[43]	HU H, WU J W, LI D, et al. Knockdown of lncRNA MALAT1 attenuates acute myocardial infarction through miR-320-Pten axis[J]. Biomed Pharmacother, 2018. DOI: 10.1016/j.biopha.2018.06.122.
[44]	ZHAO Z H, HAO W, MENG Q T, et al. Long non-coding RNA MALAT1 functions as a mediator in cardioprotective effects of fentanyl in myocardial ischemia-reperfusion injury[J]. Cell Biol Int, 2017, 41(1): 62-70. doi: 10.1002/cbin.10701
[45]	ZHAO Y J, ZHOU L, LI H, et al. Nuclear-encoded lncRNA MALAT1 epigenetically controls metabolic reprogramming in HCC cells through the mitophagy pathway[J]. Mol Ther Nucleic Acids, 2021. DOI: 10.1016/j.omtn.2020.09.040.
[46]	SHAO G Y, ZHAO Z G, ZHAO W, et al. Long non-coding RNA MALAT1 activates autophagy and promotes cell proliferation by downregulating microRNA-204 expression in gastric cancer[J]. Oncol Lett, 2020, 19(1): 805-812.
[47]	ZHANG L, FANG Y, ZHAO X Y, et al. miR-204 silencing reduces mitochondrial autophagy and ROS production in a murine AD model via the TRPML1-activated STAT3 pathway[J]. Mol Ther Nucleic Acids, 2021. DOI: 10.1016/j.omtn.2021.02.010.

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Research progress and function of mitophagy in myocardial infarction

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