ArticleCirculation. Heart failure2017
Myocardial Upregulation of Cathepsin D by Ischemic Heart Disease Promotes Autophagic Flux and Protects Against Cardiac Remodeling and Heart Failure.
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Article in Circulation. Heart failure, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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42 citing papers in PubMed, 62 citations in OpenAlex.
- Diagnostic and therapeutic innovations in myocardial infarction: a focus on mitochondrial dysfunction.Frontiers in cardiovascular medicine · 2026Review
- Proteomic Analysis of Mouse Cerebral Cortex Following Experimental Ischemic Stroke: Identifying Novel Biomarkers of Damage and Repair.Cellular and molecular neurobiology · 2025Article
- Plasma Protein Profile Associated With a Family History of Early-Onset Coronary Heart Disease.Circulation. Genomic and precision medicine · 2025Article
- Unraveling the mystery of peripartum cardiomyopathy; Cathepsin D.American heart journal plus : cardiology research and practice · 2025Article
- Low-density lipoprotein receptor-related protein 6 ameliorates cardiac hypertrophy by regulating CTSD/HSP90α signaling during pressure overload.Acta pharmacologica Sinica · 2025Article
- Cathepsin-D and outcomes in peripartum cardiomyopathy: Results from IPAC.American heart journal plus : cardiology research and practice · 2025Article
- Circulatory cathepsin K as biomarkers in older adults with sarcopenia: a case-control study.Frontiers in medicine · 2025Article
- Bioinformatics analyses reveal the autophagy-related feature biomarkers in dilated cardiomyopathy with heart failure.Frontiers in cardiovascular medicine · 2025Article
- A combined analysis of bulk RNA-seq and scRNA-seq was performed to investigate the molecular mechanisms associated with the occurrence of myocardial infarction.BMC genomics · 2024Article
- Decellularized extracellular matrix materials for treatment of ischemic cardiomyopathy.Bioactive materials · 2024Review
- Impaired autophagy flux contributes to enhanced ischemia reperfusion injury in the diabetic heart.Autophagy reports · 2024Article
- Lysosomal calcium loading promotes spontaneous calcium release by potentiating ryanodine receptors.Biophysical journal · 2023Article
- Lysosomal dysfunction in diabetic cardiomyopathy.Frontiers in aging · 2023Review
- Article
- Protein homeostasis in the aged and diseased heart.The journal of cardiovascular aging · 2023Article
- A nanoparticle probe for the imaging of autophagic flux in live mice via magnetic resonance and near-infrared fluorescence.Nature biomedical engineering · 2022Article
- The role of autophagy in cardiovascular pathology.Cardiovascular research · 2022Review
- Autophagy in the Neuronal Ceroid Lipofuscinoses (Batten Disease).Frontiers in cell and developmental biology · 2022Review
- Identification and exploration of novel M2 macrophage-related biomarkers in the development of acute myocardial infarction.Frontiers in cardiovascular medicine · 2022Article
- Ubiquitin Carboxyl-Terminal Hydrolase L1 of Cardiomyocytes Promotes Macroautophagy and Proteostasis and Protects Against Post-myocardial Infarction Cardiac Remodeling and Heart Failure.Frontiers in cardiovascular medicine · 2022Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Penglong WuFrom the Department of Cardiology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, China (P.W., M.W., J.L., X.W.); Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, Vermillion (P.W., X.W.); Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis (X.Y., F.L.); Department of Pathology, University of Alabama at Birmingham (J.Z.); Clinical Research Center and Division of Cardiology, Zhejiang University School of Medicine 2nd Affiliated Hospital, Hangzhou, China (W.Z.); Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Guangzhou, China (X.W.); and Guangzhou Institute of Oncology, Tumor Hospital, Guangzhou Medical University, China (X.W.).
Xun YuanFrom the Department of Cardiology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, China (P.W., M.W., J.L., X.W.); Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, Vermillion (P.W., X.W.); Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis (X.Y., F.L.); Department of Pathology, University of Alabama at Birmingham (J.Z.); Clinical Research Center and Division of Cardiology, Zhejiang University School of Medicine 2nd Affiliated Hospital, Hangzhou, China (W.Z.); Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Guangzhou, China (X.W.); and Guangzhou Institute of Oncology, Tumor Hospital, Guangzhou Medical University, China (X.W.).
Faqian LiFrom the Department of Cardiology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, China (P.W., M.W., J.L., X.W.); Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, Vermillion (P.W., X.W.); Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis (X.Y., F.L.); Department of Pathology, University of Alabama at Birmingham (J.Z.); Clinical Research Center and Division of Cardiology, Zhejiang University School of Medicine 2nd Affiliated Hospital, Hangzhou, China (W.Z.); Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Guangzhou, China (X.W.); and Guangzhou Institute of Oncology, Tumor Hospital, Guangzhou Medical University, China (X.W.).
Jianhua ZhangFrom the Department of Cardiology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, China (P.W., M.W., J.L., X.W.); Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, Vermillion (P.W., X.W.); Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis (X.Y., F.L.); Department of Pathology, University of Alabama at Birmingham (J.Z.); Clinical Research Center and Division of Cardiology, Zhejiang University School of Medicine 2nd Affiliated Hospital, Hangzhou, China (W.Z.); Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Guangzhou, China (X.W.); and Guangzhou Institute of Oncology, Tumor Hospital, Guangzhou Medical University, China (X.W.).
Wei ZhuFrom the Department of Cardiology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, China (P.W., M.W., J.L., X.W.); Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, Vermillion (P.W., X.W.); Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis (X.Y., F.L.); Department of Pathology, University of Alabama at Birmingham (J.Z.); Clinical Research Center and Division of Cardiology, Zhejiang University School of Medicine 2nd Affiliated Hospital, Hangzhou, China (W.Z.); Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Guangzhou, China (X.W.); and Guangzhou Institute of Oncology, Tumor Hospital, Guangzhou Medical University, China (X.W.).
Meng WeiFrom the Department of Cardiology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, China (P.W., M.W., J.L., X.W.); Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, Vermillion (P.W., X.W.); Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis (X.Y., F.L.); Department of Pathology, University of Alabama at Birmingham (J.Z.); Clinical Research Center and Division of Cardiology, Zhejiang University School of Medicine 2nd Affiliated Hospital, Hangzhou, China (W.Z.); Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Guangzhou, China (X.W.); and Guangzhou Institute of Oncology, Tumor Hospital, Guangzhou Medical University, China (X.W.).
Jingbo LiFrom the Department of Cardiology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, China (P.W., M.W., J.L., X.W.); Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, Vermillion (P.W., X.W.); Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis (X.Y., F.L.); Department of Pathology, University of Alabama at Birmingham (J.Z.); Clinical Research Center and Division of Cardiology, Zhejiang University School of Medicine 2nd Affiliated Hospital, Hangzhou, China (W.Z.); Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Guangzhou, China (X.W.); and Guangzhou Institute of Oncology, Tumor Hospital, Guangzhou Medical University, China (X.W.). xuejun.wang@usd.edu lijb@sjtu.edu.cn.
Xuejun WangFrom the Department of Cardiology, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, China (P.W., M.W., J.L., X.W.); Division of Basic Biomedical Sciences, Sanford School of Medicine of the University of South Dakota, Vermillion (P.W., X.W.); Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis (X.Y., F.L.); Department of Pathology, University of Alabama at Birmingham (J.Z.); Clinical Research Center and Division of Cardiology, Zhejiang University School of Medicine 2nd Affiliated Hospital, Hangzhou, China (W.Z.); Key Laboratory of Protein Modification and Degradation, School of Basic Medical Sciences, Guangzhou, China (X.W.); and Guangzhou Institute of Oncology, Tumor Hospital, Guangzhou Medical University, China (X.W.). xuejun.wang@usd.edu lijb@sjtu.edu.cn.
University of South Dakota · USSecond Affiliated Hospital of Zhejiang University · CNUniversity of Alabama at Birmingham · USUniversity of Minnesota · US
Funding
Ubiquitin receptors and cardiac proteotoxicityR01HL072166 · NHLBI · UNIVERSITY OF SOUTH DAKOTA · PI WANG, XUEJUN · 2003 to 2023
$6.9MThe COP9 SIgnalosome in the HeartR01HL085629 · NHLBI · UNIVERSITY OF SOUTH DAKOTA · PI WANG, XUEJUN · 2006 to 2019
$4.7MNuclear beta-catenin signaling in the heartR01HL111480 · NHLBI · UNIVERSITY OF ROCHESTER · PI LI, FAQIAN · 2012 to 2016
$1.9MThe NRF2-p62 Axis in the Cross-Talk between Proteasomal and Lysosomal DegradationR01HL131667 · NHLBI · UNIVERSITY OF SOUTH DAKOTA · PI CUI, TAIXING, WANG, XUEJUN · 2017 to 2020
$1.4MNHLBI NIH HHS R01 HL072166NHLBI NIH HHS R01 HL085629NHLBI NIH HHS R01 HL111480NHLBI NIH HHS R01 HL131667
Abstract
backgroundLysosomal dysfunction is implicated in human heart failure for which ischemic heart disease is the leading cause. Altered myocardial expression of CTSD (cathepsin D), a major lysosomal protease, was observed in human heart failure, but its pathophysiological significance has not been determined. METHODS AND
resultsWestern blot analyses revealed an increase in the precursor but not the mature form of CTSD in myocardial samples from explanted human failing hearts with ischemic heart disease, which is recapitulated in chronic myocardial infarction produced via coronary artery ligation in
conclusionsMyocardial CTSD upregulation induced by myocardial infarction protects against cardiac remodeling and malfunction, which is at least in part through promoting myocardial autophagic flux.
Indexed as
AutophagyUp-RegulationVentricular RemodelingAnimalsCathepsin DDisease Models, AnimalHeart FailureHeart VentriclesHumansMiceMice, Inbred C57BLMicroscopy, ConfocalMyocardial IschemiaMyocardiumCathepsin Dautophagyblotting, Westerncathepsin Dgene targetingmyocardial infarction
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