ArticleJournal of cellular and molecular medicine2024
miR-31-5p suppresses myocardial hypertrophy by targeting Nfatc2ip.
Article in Journal of cellular and molecular medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Integrated Genomic and Transcriptomic Analysis Reveals the Genetic Basis and Causal Association Between Obesity and Atrial Fibrillation.Diabetes, obesity & metabolism · 2026Article
- The cardiac protective human circular RNA circKLHL20_009 sponges miR-31-5p to ameliorate myocardial hypertrophy and fibrosis through suppressing β-catenin signaling.Acta pharmacologica Sinica · 2026Article
- MiR-32-3p improves ISO induced AC16 myocardial cell injury by targeting ATF4.Journal of cardiothoracic surgery · 2026Article
- Multi-Organ Physiologic Deficits During Exercise Identify Clinical and Molecular Predisposition to Heart Failure with Preserved Ejection Fraction.Circulation · 2026Article
- Article
- MicroRNAs in Heart Failure Pathogenesis and Progression: Mechanistic Control, Biomarker Potential, and Translational Perspectives.Life (Basel, Switzerland) · 2026Review
- Specific GPCRs Elicit Unique Extracellular Vesicle MiRNA Array Signatures: An Exploratory Study.bioRxiv : the preprint server for biology · 2025Article
- The Latest Advances in Omics Technology for Assessing Tissue Damage: Implications for the Study of Sudden Cardiac Death.International journal of molecular sciences · 2025Review
- miR-31-5p suppresses myocardial hypertrophy by targeting Nfatc2ip.Journal of cellular and molecular medicine · 2024Article
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4 authors.
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Abstract
Cardiac hypertrophy, worldwide known as an adaptive functional compensatory state of myocardial stress, is mainly believed to proceed to severe heart diseases, even to sudden death. Emerging studies have explored the microRNA alteration during hypertrophy. However, the mechanisms of microRNAs involved in cardiac hypertrophy are still uncertain. We studied young rats to establish abdominal aorta coarctation (AAC) for 4 weeks. With the significant downregulated cardiac function and upregulated hypertrophic biomarkers, AAC-induced rats showed enlarged myocardiocytes and alterations in microRNAs, especially downregulated miR-31-5p. miR-31-5p targets the 3'UTR of Nfatc2ip and inhibits myocardial hypertrophy in vitro and in vivo. Furthermore, we verified that Nfatc2ip is necessary and sufficient for cardiac hypertrophy in neonatal rat cardiomyocytes. Moreover, we found miR-31-5p inhibited the colocalization of Nfatc2ip and hypertrophic gene β-Mhc. Luciferase assay and ChiP-qPCR test demonstrated that Nfatc2ip binded to the core-promoter of β-Mhc and enhanced its transcriptional activity. Above all, our study found a new pathway, mir-31-5p/Nfatc2ip/β-Mhc, which is involved in cardiac hypertrophy, suggesting a potential target for intervention of cardiac hypertrophy.
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