ArticleCardiovascular research2017
MicroRNA-532 protects the heart in acute myocardial infarction, and represses prss23, a positive regulator of endothelial-to-mesenchymal transition.
Article in Cardiovascular research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 2 of them syntheses that pooled it.
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Who cites it
47 citing papers in PubMed, 2 syntheses or guidelines pooled it, 77 citations in OpenAlex.
- Advances in the study of exosomes in cardiovascular diseases.Journal of advanced research · 2024Pooled it
- Pooled it
- Myeloid cell-specific β2-adrenergic receptor deletion improves early cardiac injury resolution via de-repression of Anxa1.Theranostics · 2026Article
- Loss of primary cilia promotes EphA2-mediated endothelial-to-mesenchymal transition in the ovarian tumor microenvironment.Molecular oncology · 2025Article
- Shifting Shapes: The Endothelial-to-Mesenchymal Transition as a Driver for Cancer Progression.International journal of molecular sciences · 2025Review
- Critical analysis of descriptive microRNA data in the translational research on cardioprotection and cardiac repair: lost in the complexity of bioinformatics.Basic research in cardiology · 2025Review
- Mechanistic insights and emerging therapeutic strategies targeting endothelial dysfunction in cardiovascular diseases.Archives of pharmacal research · 2025Review
- MicroRNA-197-3p Transfection: Variations in Cardiomyocyte Gene Expression with Anaesthetics Drugs in a Model of Hypoxia/Reperfusion.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Gene Expression Signatures of Smoking and Acute Myocardial Infarction: A Blood Transcriptome Analysis.Mediators of inflammation · 2025Article
- MicroRNA delivery based on nanoparticles of cardiovascular diseases.Molecular and cellular biochemistry · 2024Review
- Pericardial Fluid Accumulates microRNAs That Regulate Heart Fibrosis after Myocardial Infarction.International journal of molecular sciences · 2024Article
- Circular RNAs: a small piece in the heart failure puzzle.Functional & integrative genomics · 2024Review
- High glutamine increases stroke risk by inducing the endothelial-to-mesenchymal transition in moyamoya disease.MedComm · 2024Article
- Exosomal miR-532-5p induced by long-term exercise rescues blood-brain barrier function in 5XFAD mice via downregulation of EPHA4.Aging cell · 2023Article
- The diagnostic value of circulating miR-532-5p in patients with asymptomatic carotid artery stenosis and its predictive significance for the occurrence of cerebral ischaemic events.Archives of medical science : AMS · 2023Article
- MiR-150 blunts cardiac dysfunction in mice with cardiomyocyte loss of βCell death discovery · 2022Article
- Lymphangiocrine signals are required for proper intestinal repair after cytotoxic injury.Cell stem cell · 2022Article
- MiR-150 Attenuates Maladaptive Cardiac Remodeling Mediated by Long Noncoding RNA MIAT and Directly Represses ProfibroticCirculation. Heart failure · 2022Article
- Research Progress of Traditional Chinese Medicine in Treatment of Myocardial fibrosis.Frontiers in pharmacology · 2022Review
- Endocardial Endothelial Dysfunction and Unknown Polymorphic Composite Accumulation in Heart Failure.Biomedicines · 2021Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
aimsAcute myocardial infarction (MI) leads to cardiac remodelling and development of heart failure. Insufficient myocardial capillary density after MI is considered a critical determinant of this process. MicroRNAs (miRs), negative regulators of gene expression, have emerged as important players in MI. We previously showed that miR-532-5p (miR-532) is up-regulated by the β-arrestin-biased β-adrenergic receptor antagonist (β-blocker) carvedilol, which activates protective pathways in the heart independent of G protein-mediated second messenger signalling. Here, we hypothesize that β2-adrenergic receptor/β-arrestin-responsive miR-532 confers cardioprotection against MI. METHODS AND
resultsUsing cultured cardiac endothelial cell (CEC) and in vivo approaches, we show that CECs lacking miR-532 exhibit increased transition to a fibroblast-like phenotype via endothelial-to-mesenchymal transition (EndMT), while CECs over-expressing miR-532 display decreased EndMT. We also demonstrate that knockdown of miR-532 in mice causes abnormalities in cardiac structure and function as well as reduces CEC proliferation and cardiac vascularization after MI. Mechanistically, cardioprotection elicited by miR-532 is in part attributed to direct repression of a positive regulator of maladaptive EndMT, prss23 (a protease serine 23) in CECs.
conclusionsIn conclusion, these findings reveal a pivotal role for miR-532-prss23 axis in regulating CEC function after MI, and this novel axis could be suitable for therapeutic intervention in ischemic heart disease.
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