ArticleCirculation research2018
miR-146a Suppresses SUMO1 Expression and Induces Cardiac Dysfunction in Maladaptive Hypertrophy.
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 63 papers.
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Who cites it
63 citing papers in PubMed, 95 citations in OpenAlex.
- Decoding miRNA‑146a: Mechanisms of action in cardiovascular diseases and endocrine metabolic disorders (Review).International journal of molecular medicine · 2026Review
- miR-146a Deficiency Ablates β-Aminopropionitrile-Induced Thoracic Aortic Aneurysmal Rupture in Mice.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Loss of miR-146a induces cardiomyocyte proliferation after myocardial infarction through targeting Kctd15.Journal of molecular medicine (Berlin, Germany) · 2026Article
- The Landscape of SERCA2 in Cardiovascular Diseases: Expression Regulation, Therapeutic Applications, and Emerging Roles.Biomolecules · 2026Review
- Potential Biomarker and Therapeutic Tools for Pathological Cardiac Hypertrophy and Heart Failure: Extracellular Vesicles.International journal of molecular sciences · 2025Review
- Allosteric Modulation of SERCA Pumps in Health and Disease: Structural Dynamics, Posttranslational Modifications, and Therapeutic Potential.Journal of molecular biology · 2025Review
- Recent advances in the roles of extracellular vesicles in cardiovascular diseases: pathophysiological mechanisms, biomarkers, and cell-free therapeutic strategy.Molecular medicine (Cambridge, Mass.) · 2025Review
- Evaluation of miR-146a as a potential biomarker for diagnosis of cardiotoxicity induced by chemotherapy in patients with breast cancer.Journal of research in medical sciences : the official journal of Isfahan University of Medical Sciences · 2025Article
- Unraveling the Impact of miR-146a in Pulmonary Arterial Hypertension Pathophysiology and Right Ventricular Function.International journal of molecular sciences · 2024Article
- Cell Type-Specific Extracellular Vesicles and Their Impact on Health and Disease.International journal of molecular sciences · 2024Review
- Extracellular vesicles as tools and targets in therapy for diseases.Signal transduction and targeted therapy · 2024Review
- Exercise mediates myocardial infarction via non-coding RNAs.Frontiers in cardiovascular medicine · 2024Review
- Crosstalk between ubiquitin ligases and ncRNAs drives cardiovascular disease progression.Frontiers in immunology · 2024Review
- Extracellular vesicular microRNAs and cardiac hypertrophy.Frontiers in endocrinology · 2024Review
- MicroRNAs Targeting Critical Molecular Pathways in Diabetic Cardiomyopathy Emerging Valuable for Therapy.Cardiovascular & hematological agents in medicinal chemistry · 2024Review
- Mettl13 protects against cardiac contractile dysfunction by negatively regulating C-Cbl-mediated ubiquitination of SERCA2a in ischemic heart failure.Science China. Life sciences · 2023Article
- Selected miRNA and Psoriasis-Cardiovascular Disease (CVD)-Overweight/Obesity Network-A Pilot Study.International journal of molecular sciences · 2023Article
- Research progress on post-translational modification of proteins and cardiovascular diseases.Cell death discovery · 2023Review
- Cardiac Biomarkers and Their Role in Identifying Increased Risk of Cardiovascular Complications in COVID-19 Patients.Diagnostics (Basel, Switzerland) · 2023Review
- Identification of key biomarkers associated with immune cells infiltration for myocardial injury in dermatomyositis by integrated bioinformatics analysis.Arthritis research & therapy · 2023Article
3 more citing papers are in PubMed but not listed here.
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
rationaleAbnormal SUMOylation has emerged as a characteristic of heart failure (HF) pathology. Previously, we found reduced SUMO1 (small ubiquitin-like modifier 1) expression and SERCA2a (sarcoplasmic reticulum Ca
objectiveTo examine miR-146a-mediated SUMO1 regulation and its consequent effects on cardiac morphology and function. METHODS AND
resultsIn this study, miR-146a was identified as a SUMO1-targeting microRNA in the heart. A strong correlation was observed between miR-146a and SUMO1 expression in failing mouse and human hearts. miR-146a was manipulated in cardiomyocytes through AAV9 (adeno-associated virus serotype 9)-mediated gene delivery, and cardiac morphology and function were analyzed by echocardiography and hemodynamics. Overexpression of miR-146a reduced SUMO1 expression, SERCA2a SUMOylation, and cardiac contractility in vitro and in vivo. The effects of miR-146a inhibition on HF pathophysiology were examined by transducing a tough decoy of miR-146a into mice subjected to transverse aortic constriction. miR-146a inhibition improved cardiac contractile function and normalized SUMO1 expression. The regulatory mechanisms of miR-146a upregulation were elucidated by examining the major miR-146a-producing cell types and transfer mechanisms. Notably, transdifferentiation of fibroblasts triggered miR-146a overexpression and secretion through extracellular vesicles, and the extracellular vesicle-associated miR-146a transfer was identified as the causative mechanism of miR-146a upregulation in failing cardiomyocytes. Finally, extracellular vesicles isolated from failing hearts were shown to contain high levels of miR-146a and exerted negative effects on the SUMO1/SERCA2a signaling axis and hence cardiomyocyte contractility.
conclusionsTaken together, our results show that miR-146a is a novel regulator of the SUMOylation machinery in the heart, which can be targeted for therapeutic intervention.
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