ArticleCell research2012
Cardiomyocyte overexpression of miR-27b induces cardiac hypertrophy and dysfunction in mice.
Article in Cell research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers, 3 of them syntheses that pooled it.
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Who cites it
106 citing papers in PubMed, 3 syntheses or guidelines pooled it, 207 citations in OpenAlex.
- A meta-analysis of the diagnostic value of microRNA for hypertensive left ventricular hypertrophy.Frontiers in cardiovascular medicine · 2022Pooled it
- A meta-analysis of microRNA expression profiling studies in heart failure.Heart failure reviews · 2021Pooled it
- Differences in the cargos and functions of exosomes derived from six cardiac cell types: a systematic review.Stem cell research & therapy · 2019Pooled it
- Vardenafil Alleviates Doxorubicin-Induced Cardiotoxicity Associated with Restoration of the AMPK/SIRT1 Signaling Pathway.Biomedicines · 2026Article
- Hypoxia-driven microRNA-27b underlies pathologic cardiac endoreplication in heart disease.Signal transduction and targeted therapy · 2026Article
- 20(S)-protopanaxatriol ameliorates cardiac hypertrophy by activating the AMPK/PGC-1α/PPARγ signaling pathway.Journal of ginseng research · 2026Article
- Interleukin 11-Induced MicroRNAs as Functional Mediators and Circulating Biomarkers of Cardiac Fibrosis.Circulation research · 2026Article
- The Heart's Small Molecules: The Importance of MicroRNAs in Cardiovascular Health.Journal of clinical medicine · 2025Review
- Anticoagulation Therapies and microRNAs in Heart Failure.Biomolecules · 2025Review
- Interplay Between TGF-β Signaling and MicroRNA in Diabetic Cardiomyopathy.Cardiovascular drugs and therapy · 2025Review
- Managing cardiovascular events, hyperglycemia, and obesity in type 2 diabetes through microRNA regulation linked to glucagon-like peptide-1 receptor agonists.Diabetology & metabolic syndrome · 2025Review
- The crucial relationship between miRNA-27 and CSE/HInternational journal of medical sciences · 2024Article
- Peripheral blood mononuclear cells expression of miR-200c, miR-125b, miR-27b, miR-203, and miR-155 in patients with significant or insignificant coronary artery stenosis.Scientific reports · 2023Article
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- A high-throughput drug screening identifies luteolin as a therapeutic candidate for pathological cardiac hypertrophy and heart failure.Frontiers in cardiovascular medicine · 2023Article
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- MicroRNA-27b-3p down-regulates FGF1 and aggravates pathological cardiac remodelling.Cardiovascular research · 2022Article
- Review
- Network analysis of atherosclerotic genes elucidates druggable targets.BMC medical genomics · 2022Article
46 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent studies have begun to reveal critical roles of microRNAs (miRNAs) in the pathogenesis of cardiac hypertrophy and dysfunction. In this study, we tested whether a transforming growth factor-β (TGF-β)-regulated miRNA played a pivotal role in the development of cardiac hypertrophy and heart failure (HF). We observed that miR-27b was upregulated in hearts of cardiomyocyte-specific Smad4 knockout mice, which developed cardiac hypertrophy. In vitro experiments showed that the miR-27b expression could be inhibited by TGF-β1 and that its overexpression promoted hypertrophic cell growth, while the miR-27b suppression led to inhibition of the hypertrophic cell growth caused by phenylephrine (PE) treatment. Furthermore, the analysis of transgenic mice with cardiomyocyte-specific overexpression of miR-27b revealed that miR-27b overexpression was sufficient to induce cardiac hypertrophy and dysfunction. We validated the peroxisome proliferator-activated receptor-γ (PPAR-γ) as a direct target of miR-27b in cardiomyocyte. Consistently, the miR-27b transgenic mice displayed significantly lower levels of PPAR-γ than the control mice. Furthermore, in vivo silencing of miR-27b using a specific antagomir in a pressure-overload-induced mouse model of HF increased cardiac PPAR-γ expression, attenuated cardiac hypertrophy and dysfunction. The results of our study demonstrate that TGF-β1-regulated miR-27b is involved in the regulation of cardiac hypertrophy, and validate miR-27b as an efficient therapeutic target for cardiac diseases.
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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.