ArticleCirculation research2018
AMPKα2 Protects Against the Development of Heart Failure by Enhancing Mitophagy via PINK1 Phosphorylation.
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Article in Circulation research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 206 papers, 2 of them syntheses that pooled it.
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206citing papers in PubMed, 2 pooled it
12.9field-weighted citation impact, top 1% of its field
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Who cites it
206 citing papers in PubMed, 2 syntheses or guidelines pooled it, 314 citations in OpenAlex.
- Reprogramming heart failure: physiological orchestration and mechanistic decoding of exercise benefits.BMC cardiovascular disorders · 2025Pooled it
- Mitochondrial dysfunction in cardiovascular disease: Towards exercise regulation of mitochondrial function.Frontiers in physiology · 2023Pooled it
- Crosstalk between ubiquitination and other post-translational modifications in cardiovascular diseases.iScience · 2026Review
- Mitochondrial Distress Signals at the Heart-Liver Interface: Molecular Links Between MASLD and Heart Failure.International journal of molecular sciences · 2026Review
- Mechanisms and Therapeutic Potential of Targeting Mitophagy in Neurodegenerative Diseases.Molecular neurobiology · 2026Review
- P2Y12-AMPKα2 signaling contributes to cardiomyocyte senescence in doxorubicin-induced heart failure.Molecular and cellular biochemistry · 2026Article
- L-Arginine effectively alleviates doxorubicin-induced cardiac dysfunction by inhibiting myocardial fibrosis.Molecular biology reports · 2026Article
- Biology of HDL: From Structural Heterogeneity to Dysfunctional Remodeling in Cardiovascular Disease and Comorbidities.Antioxidants (Basel, Switzerland) · 2026Review
- Mitochondrial quality control in human ageing and longevity.Nature metabolism · 2026Review
- FGF21-FGFR1 signaling protects against cardiac hypertrophy by regulating PINK1-mediated mitophagy pathway.Journal of advanced research · 2026Article
- AMPK Signalling in Heart Failure: From Metabolic Sensor to Context-Dependent Therapeutic Target.Biomedicines · 2026Review
- Post-translational modifications of mitochondrion-related proteins: integrative orchestrators of cell fate networks in cardiovascular disease.Cell communication and signaling : CCS · 2026Review
- Betulin Protects Against Cardiac Hypertrophy by Improving AMPK/Nrf2-Dependent Mitochondrial Function.Phytotherapy research : PTR · 2026Article
- Mitophagy in cardiovascular diseases: a literature review.Cardiovascular diagnosis and therapy · 2026Review
- Regulation of mitochondrial biogenesis and energy metabolism in the heart.Chinese medical journal · 2026Review
- The Metabolic Role of Mitochondria in the Perinatal Cardiac Development and Cardiovascular Diseases.Exploration (Beijing, China) · 2026Review
- Targeting the AMPK Pathway with Natural Products for Heart Failure: A Systematic Review of Preclinical Evidence.Biomedicines · 2026Review
- Advances in natural compounds modulating autophagy for the therapeutic intervention of heart failure.Molecular and cellular biochemistry · 2026Review
- Activating protein kinases to treat diseases: Current understanding and future challenges.Acta pharmaceutica Sinica. B · 2026Review
- Mitophagy in the pathogenesis and management of disease.Cell research · 2026Review
146 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 1 institution in 1 country.
Bei WangFrom the Division of Cardiology, Department of Internal Medicine and Gene Therapy Center, Tongji Hospital, Tongji Medical College (B.W., J.N., L.W., Z.W.,C.C., D.W.W.), Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders (B.W., J.N., L.W., Z.W.,C.C., D.W.W.), and Department of Rheumatology and Immunology, Tongji Hospital, Tongji Medical College (B.W., Y.H., L.D.), Huazhong University of Science and Technology, Wuhan, China; and Center for Molecular and Translational Medicine, Georgia State University, Atlanta (M.-H.Z.).
Jiali NieFrom the Division of Cardiology, Department of Internal Medicine and Gene Therapy Center, Tongji Hospital, Tongji Medical College (B.W., J.N., L.W., Z.W.,C.C., D.W.W.), Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders (B.W., J.N., L.W., Z.W.,C.C., D.W.W.), and Department of Rheumatology and Immunology, Tongji Hospital, Tongji Medical College (B.W., Y.H., L.D.), Huazhong University of Science and Technology, Wuhan, China; and Center for Molecular and Translational Medicine, Georgia State University, Atlanta (M.-H.Z.).
Lujin WuFrom the Division of Cardiology, Department of Internal Medicine and Gene Therapy Center, Tongji Hospital, Tongji Medical College (B.W., J.N., L.W., Z.W.,C.C., D.W.W.), Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders (B.W., J.N., L.W., Z.W.,C.C., D.W.W.), and Department of Rheumatology and Immunology, Tongji Hospital, Tongji Medical College (B.W., Y.H., L.D.), Huazhong University of Science and Technology, Wuhan, China; and Center for Molecular and Translational Medicine, Georgia State University, Atlanta (M.-H.Z.).
Yangyang HuFrom the Division of Cardiology, Department of Internal Medicine and Gene Therapy Center, Tongji Hospital, Tongji Medical College (B.W., J.N., L.W., Z.W.,C.C., D.W.W.), Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders (B.W., J.N., L.W., Z.W.,C.C., D.W.W.), and Department of Rheumatology and Immunology, Tongji Hospital, Tongji Medical College (B.W., Y.H., L.D.), Huazhong University of Science and Technology, Wuhan, China; and Center for Molecular and Translational Medicine, Georgia State University, Atlanta (M.-H.Z.).
Zheng WenFrom the Division of Cardiology, Department of Internal Medicine and Gene Therapy Center, Tongji Hospital, Tongji Medical College (B.W., J.N., L.W., Z.W.,C.C., D.W.W.), Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders (B.W., J.N., L.W., Z.W.,C.C., D.W.W.), and Department of Rheumatology and Immunology, Tongji Hospital, Tongji Medical College (B.W., Y.H., L.D.), Huazhong University of Science and Technology, Wuhan, China; and Center for Molecular and Translational Medicine, Georgia State University, Atlanta (M.-H.Z.).
Lingli DongFrom the Division of Cardiology, Department of Internal Medicine and Gene Therapy Center, Tongji Hospital, Tongji Medical College (B.W., J.N., L.W., Z.W.,C.C., D.W.W.), Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders (B.W., J.N., L.W., Z.W.,C.C., D.W.W.), and Department of Rheumatology and Immunology, Tongji Hospital, Tongji Medical College (B.W., Y.H., L.D.), Huazhong University of Science and Technology, Wuhan, China; and Center for Molecular and Translational Medicine, Georgia State University, Atlanta (M.-H.Z.).
Ming-Hui ZouFrom the Division of Cardiology, Department of Internal Medicine and Gene Therapy Center, Tongji Hospital, Tongji Medical College (B.W., J.N., L.W., Z.W.,C.C., D.W.W.), Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders (B.W., J.N., L.W., Z.W.,C.C., D.W.W.), and Department of Rheumatology and Immunology, Tongji Hospital, Tongji Medical College (B.W., Y.H., L.D.), Huazhong University of Science and Technology, Wuhan, China; and Center for Molecular and Translational Medicine, Georgia State University, Atlanta (M.-H.Z.).
Chen ChenFrom the Division of Cardiology, Department of Internal Medicine and Gene Therapy Center, Tongji Hospital, Tongji Medical College (B.W., J.N., L.W., Z.W.,C.C., D.W.W.), Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders (B.W., J.N., L.W., Z.W.,C.C., D.W.W.), and Department of Rheumatology and Immunology, Tongji Hospital, Tongji Medical College (B.W., Y.H., L.D.), Huazhong University of Science and Technology, Wuhan, China; and Center for Molecular and Translational Medicine, Georgia State University, Atlanta (M.-H.Z.). dwwang@tjh.tjmu.edu.cn chenchen@tjh.tjmu.edu.cn.
Dao Wen WangFrom the Division of Cardiology, Department of Internal Medicine and Gene Therapy Center, Tongji Hospital, Tongji Medical College (B.W., J.N., L.W., Z.W.,C.C., D.W.W.), Hubei Key Laboratory of Genetics and Molecular Mechanisms of Cardiological Disorders (B.W., J.N., L.W., Z.W.,C.C., D.W.W.), and Department of Rheumatology and Immunology, Tongji Hospital, Tongji Medical College (B.W., Y.H., L.D.), Huazhong University of Science and Technology, Wuhan, China; and Center for Molecular and Translational Medicine, Georgia State University, Atlanta (M.-H.Z.). dwwang@tjh.tjmu.edu.cn chenchen@tjh.tjmu.edu.cn.
Georgia State University · US
Funding
Reactive Nitrogen species and Diabetic Endothelial DysfunctionR01HL079584 · NHLBI · UNIVERSITY OF TENNESSEE KNOXVILLE · PI ZOU, MING-HUI · 2004 to 2021
$7.3MInflammasome and unstable atherosclerotic plaquesR01HL089920 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2008 to 2022
$6.9MAMP-Activated Protein Kinase in DiabetesR01HL080499 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2006 to 2019
$5.8MControlling VSMC Proliferation and MigrationR01HL110488 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2011 to 2020
$3.9MOxidant stress and diabetic endothelial dysfunctionR01HL074399 · NHLBI · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2005 to 2013
$3.2MFUNDC1 and diabetic cardiomyopathyR01HL137371 · NHLBI · GEORGIA STATE UNIVERSITY · PI XIE, ZHONGLIN, ZOU, MING-HUI · 2017 to 2020
$2.8MMKP1, VSMC, and Vascular RemodelingR01HL140954 · NHLBI · GEORGIA STATE UNIVERSITY · PI SONG, PING, ZOU, MING-HUI · 2018 to 2021
$2.8MAutophagy and VSMC migrationR01HL132500 · NHLBI · GEORGIA STATE UNIVERSITY · PI XIE, ZHONGLIN, ZOU, MING-HUI · 2016 to 2019
$2.7MSuppression of Autophagy-Dependent Clearance Mitochondria in Type 2 DiabetesR01HL128014 · NHLBI · GEORGIA STATE UNIVERSITY · PI XIE, ZHONGLIN, ZOU, MING-HUI · 2015 to 2018
$2.4MLiver kinase B1 in angiogenesisR01CA213022 · NCI · GEORGIA STATE UNIVERSITY · PI ZOU, MING-HUI · 2017 to 2021
$2.3MSirt1, Vascular Aging, and Aortic AneurysmR01AG047776 · NIA · UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR · PI ZOU, MING-HUI · 2014 to 2018
$1.5MNCI NIH HHS R01 CA213022NHLBI NIH HHS R01 HL074399NHLBI NIH HHS R01 HL079584NHLBI NIH HHS R01 HL080499NHLBI NIH HHS R01 HL089920NHLBI NIH HHS R01 HL110488NHLBI NIH HHS R01 HL128014NHLBI NIH HHS R01 HL132500NHLBI NIH HHS R01 HL137371NHLBI NIH HHS R01 HL140954NIA NIH HHS R01 AG047776
Abstract
rationaleMitochondrial dysfunction plays an important role in heart failure (HF). However, the molecular mechanisms regulating mitochondrial functions via selective mitochondrial autophagy (mitophagy) are poorly understood.
objectiveWe sought to determine the role of AMPK (AMP-activated protein kinase) in selective mitophagy during HF. METHODS AND
resultsAn isoform shift from AMPKα2 to AMPKα1 was observed in failing heart samples from HF patients and transverse aortic constriction-induced mice, accompanied by decreased mitophagy and mitochondrial function. The recombinant adeno-associated virus Serotype 9-mediated overexpression of AMPKα2 in mouse hearts prevented the development of transverse aortic constriction-induced chronic HF by increasing mitophagy and improving mitochondrial function. In contrast, AMPKα2
conclusionsIn failing hearts, the dominant AMPKα isoform switched from AMPKα2 to AMPKα1, which accelerated HF. The results show that phosphorylation of Ser495 in PINK1 by AMPKα2 was essential for efficient mitophagy to prevent the progression of HF.
Indexed as
MitophagyAMP-Activated Protein Kinase KinasesAnimalsCells, CulturedHeart FailureHumansIsoenzymesMiceMitochondria, HeartMyocytes, CardiacPhosphorylationProtein KinasesPTEN-Induced Putative KinaseAMP-Activated Protein Kinase KinasesIsoenzymesProtein KinasesPTEN-Induced Putative Kinaseautophagyconstrictionheart failuremicemitochondria
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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 Socratic graph.