ArticleCirculation2013
MiR-378 controls cardiac hypertrophy by combined repression of mitogen-activated protein kinase pathway factors.
Article in Circulation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 140 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
140 citing papers in PubMed, 1 synthesis or guideline pooled it, 236 citations in OpenAlex.
- Prognostic significance of miR-378 in cancers: a meta-analysis.BMC cancer · 2025Pooled it
- Effect of plasma MicroRNA on antihypertensive response to beta blockers in the Pharmacogenomic Evaluation of Antihypertensive Responses (PEAR) studies.European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences · 2019Trial
- Acute resistance exercise modulates microRNA expression profiles: Combined tissue and circulatory targeted analyses.PloS one · 2017Trial
- ZBED6 deficiency drives pathological cardiac hypertrophy through MEOX1-ERK1/2-dependent autophagy dysfunction.PLoS genetics · 2026Article
- KCNE2 upregulation improves cardiac function by inhibiting Smurf1-mediated SERCA2a degradation in diabetic cardiomyopathy in mice.Acta pharmacologica Sinica · 2026Article
- Exercise-related microRNAs in Caenorhabditis elegans regulate calcium homeostasis and mitochondrial dynamics: Conserved pathways, divergent microRNAs.The FEBS journal · 2026Article
- Are RNA Therapies a Solid Foundation or a Frontier Yet to Be Conquered?International journal of molecular sciences · 2026Review
- Advances in MicroRNA-Based Therapies for Cardiac Repair: Emerging Strategies for Treating Myocardial Infarction.Molecular and cellular biochemistry · 2026Review
- Bridging miRNA Research with Clinical Applications in Cardiovascular Diseases: Advances in Delivery Systems and Therapeutic Strategies.Mini reviews in medicinal chemistry · 2026Review
- Potential Biomarker and Therapeutic Tools for Pathological Cardiac Hypertrophy and Heart Failure: Extracellular Vesicles.International journal of molecular sciences · 2025Review
- New Biomarkers in the Diagnosis and Prognosis of Dilated Cardiomyopathy: Pro-Resolving Lipids and miRNAs.Cells · 2025Article
- Plasma extracellular vesicle cargo microRNAs are associated with heart failure and cardiovascular death following acute coronary syndrome.Extracellular vesicle · 2025Article
- Review
- Extracellular vesicles derived from bone marrow mesenchymal stem cells regulate SREBF2/HMGB1 axis by transporting miR-378a-3p to inhibit ferroptosis in intestinal ischemia-reperfusion injury.Cell death discovery · 2025Article
- High-dimensional mediation analysis for longitudinal mediators and survival outcomes.Briefings in bioinformatics · 2025Article
- Macrophage-derived extracellular vesicles regulate skeletal stem/progenitor Cell lineage fate and bone deterioration in obesity.Bioactive materials · 2024Article
- Non-Coding RNA-Targeted Therapy: A State-of-the-Art Review.International journal of molecular sciences · 2024Review
- MicroRNA-30d and -483-3p for bi-ventricular remodelling and miR-126-3p for pulmonary hypertension in advanced heart failure.ESC heart failure · 2024Article
- Extracellular vesicular microRNAs and cardiac hypertrophy.Frontiers in endocrinology · 2024Review
- Article
80 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
No grant is acknowledged in the PubMed record.
Abstract
backgroundSeveral microRNAs (miRs) have been shown to regulate gene expression in the heart, and dysregulation of their expression has been linked to cardiac disease. miR-378 is strongly expressed in the mammalian heart but so far has been studied predominantly in cancer, in which it regulates cell survival and tumor growth. METHODS AND
resultsHere, we report tight control of cardiomyocyte hypertrophy through miR-378. In isolated primary cardiomyocytes, miR-378 was found to be both necessary and sufficient to repress cardiomyocyte hypertrophy. Bioinformatic prediction suggested that factors of the mitogen-activated protein kinase (MAPK) pathway are enriched among miR-378 targets. Using mRNA and protein expression analysis along with luciferase assays, we validated 4 key components of the MAPK pathway as targets of miR-378: MAPK1 itself, insulin-like growth factor receptor 1, growth factor receptor-bound protein 2, and kinase suppressor of ras 1. RNA interference with these targets prevented the prohypertrophic effect of antimiR-378, suggesting their functional relation with miR-378. Because miR-378 significantly decreases in cardiac disease, we sought to compensate for its loss through adeno-associated virus-mediated, cardiomyocyte-targeted expression of miR-378 in an in vivo model of cardiac hypertrophy (pressure overload by thoracic aortic constriction). Restoration of miR-378 levels significantly attenuated thoracic aortic constriction-induced cardiac hypertrophy and improved cardiac function.
conclusionsOur data identify miR-378 as a regulator of cardiomyocyte hypertrophy, which exerts its activity by suppressing the MAPK signaling pathway on several distinct levels. Restoration of disease-associated loss of miR-378 through cardiomyocyte-targeted adeno-associated virus-miR-378 may prove to be an effective therapeutic strategy in myocardial disease.
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Registered trials
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 OpenQuestion graph.