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Aging and disease    2020, Vol. 11 Issue (2) : 419-437     DOI: 10.14336/AD.2019.0518
Review Article |
Role of Mitophagy in Cardiovascular Disease
Yibo Yang, Tianyi Li, Zhibo Li, Ning Liu, Youyou Yan, Bin Liu*
Department of Cardiology, The Second Hospital of Jilin University, Changchun 130041, China
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Abstract  

Cardiovascular disease is the leading cause of mortality worldwide, and mitochondrial dysfunction is the primary contributor to these disorders. Recent studies have elaborated on selective autophagy-mitophagy, which eliminates damaged and dysfunctional mitochondria, stabilizes mitochondrial structure and function, and maintains cell survival and growth. Numerous recent studies have reported that mitophagy plays an important role in the pathogenesis of various cardiovascular diseases. This review summarizes the mechanisms underlying mitophagy and advancements in studies on the role of mitophagy in cardiovascular disease.

Keywords cardiomyocyte      cardiovascular disease      mitochondria      mitophagy     
Corresponding Authors: Liu Bin   
About author:

These authors contributed equally to this work.

Just Accepted Date: 22 July 2019   Issue Date: 13 March 2020
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Cite this article:   
Yang Yibo,Li Tianyi,Li Zhibo, et al. Role of Mitophagy in Cardiovascular Disease[J]. Aging and disease, 2020, 11(2): 419-437.
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http://www.aginganddisease.org/EN/10.14336/AD.2019.0518     OR
Figure 1.  The mechanisms underlying mitophagy. (A) An overview of the mechanisms underlying mitophagy. (B) Step1: Phagophores are formed by the isolated membrane and LC3. Step2: Thereafter, through LC3 adaptors and LC3 receptors, damaged mitochondria can be recognized and form mitophagosomes. The detailed mechanism can be divided into six stages. a. CHDH accumulates on the outer mitochondrial membrane (OMM) and interacts with p62 and binds with LC3. b. PINK1 accumulates on the OMM, phosphorylates Parkin and Mfn2, thus recruiting Parkin to the OMM, and Parkin helps generate ubiquitin chains on the OMM, which can recognize p62 and bind with LC3. c. PINK1 phosphorylates ubiquitin on the OMM and LC3 adapters can bind with it. d. LC3 directly recognizes BNIP3 or Nix through LIR, and phosphorylation of LIR in BNIP3 promotes the interaction between BNIP3 and LC3. e. Dephosphorylation of FUNDC1 restores its ability to interact with LC3 through LIR. f. AMBRA1, Bcl2L13, and cardiophospholipids directly recognize LC3 through LIR. Step3: Mitophagosomes and lysosomes fuse into mitolysosomes.
DiseasesRepresentativesMechanismsEffectsReferences
MicroRNAs
I/RMiR-410Mitophagy-damage[165]
I/RMiR-137BNIP3/FUNDC1--[166]
Cardiac Lipotoxicity, DCMMiR-133aNix-protection[167]

Clinical drugs and chemical reagents

I/RMelatoninPINK1/Parkin-protection[168]
DCMMelatoninPINK1/Parkin+protection[169]
ASMelatoninPINK1/Parkin+protection[170]
I/RSimvastatinParkin/P62+protection[171]
I/RLiraglutideParkin+protection[172]
I/RZinePINK1+protection[173]
I/RSevoflurane postconditioningParkin-protection[174]
I/RTEMPOL preconditioningPINK1/Parkin+protection[175]
HFCurcuminBNIP3-protection[176]
CardiotoxicityEllagic acidBNIP3-protection[177]
StrokeTunicamycin and thapsigarginMitophagy+protection[178]
StrokePeroxynitritePINK1/Parkin+damage[179]
StrokeNaringinParkin-protection[180]

Signal pathways

ASNR4A1/CaMKII activationParkin+damage[145]
StrokeMAPK-ERK-CREB blockadeMfn2-damage[181]
I/RRab5 endosomal pathway activationParkin+protection[182].
I/RP53/TIGAR activationBNIP3-damage[183]
HFJNK/FOXO3a activationBNIP3+damage[184].

Activators/inhibitors, genes knock in/out

I/RSTAT1 activationMitophagy-damage[185]
ASPINK1/Parkin knockoutPINK1/Parkin-damage[146, 147]
I/RGPER activationPINK1/Parkin-protection[93]
I/RALDH2 activationPINK1/Parkin-protection[186]
DCMSirt3 overexpressionParkin+protection[187]
DCMMst1 knockoutParkin+protection[188]
HFBAG3 knockdownParkin-damage[189]
ASF13APINK1/Parkin-protection[190]
HFCsAPINK1/Parkin-protection[191]
HFAkt2 knockoutBNIP3/PINK1/Parkin+protection[192]
StrokeNix knockoutNix-damage[161]
I/RDUSP1 activationBNIP3-protection[98]
HFSWI/SNF deletionBNIP3+damage[193]
I/RFUNDC1 knockoutFUNDC1-damage[96]

Environmental stimuli

I/RMild hypothermiaParkin-protection[194]
I/RHypoxic preconditioningFUNDC1+protection[96]
Myocardial inflammatoryAcute exerciseBNIP3+protection[80]
I/RExercise preconditioningParkin+protection[195]
StrokeAcidic postconditioningMitophagy+protection[196]
StrokeRemote ischemic post conditioningParkin+protection[197]
Table1  Therapeutic application of mitophagy.
Figure 2.  The graphical abstract. Mitophagy plays an important role in cardiovascular disease, and the degree of mitophagy can be detected via TEM, western blotting, fluorescence labeling, and mitochondrial mass determination, and the related molecular mechanism depends on PINK1/Parkin, CHDH, Nix/BNIP3, FUNDC1, etc. Mitophagy is related with certain physiological and pathological phenomena including stress, cellular defense, maintenance of cellular homeostasis, regulation of cell growth and development, and aging; these phenomena are also involved in the pathogenesis of cardiovascular diseases including ischemic heart disease, diabetic cardiomyopathy, heart failure, hypertension, atherosclerosis, arrhythmia, and stroke, and these diseases are closely associated with mitophagy. Therefore, certain factors including microRNAs, clinical drugs and chemical reagents, signaling pathways, activators/inhibitors and gene knock in/out, and environmental stimuli can regulate the level of mitophagy to alter the progression of these diseases.
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