ArticleActa biochimica et biophysica Sinica2022
miR-96-5p regulates myocardial infarction-induced cardiac fibrosis via Smad7/Smad3 pathway.
Article in Acta biochimica et biophysica Sinica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Epigenetic Regulatory Networks in Cardiac Fibrosis: Therapeutic Targets, Crosstalk, and Future Directions.Drug design, development and therapy · 2026Review
- Cardiovascular toxicity induced by immune checkpoint inhibitors: mechanisms linking immune dysregulation and myocardial fibrosis.American journal of clinical and experimental immunology · 2026Review
- Exploring the Role of Transcriptomics, Proteomics, and Machine Learning in HPV Infection and Cardiovascular Disease.Biomedicines · 2025Review
- The Zebrafish miR-183 Family Regulates Endoderm Convergence and Heart Development via S1Pr2 Signaling Pathway.Biomolecules · 2025Article
- SMAD7: riding on fibrosis-limiting routes and beyond.EMBO molecular medicine · 2025Review
- Sevoflurane alleviates hypoxia/reoxygenation-induced myocardial cell injury by regulating miR-93-5p.Toxicology research · 2025Article
- ncRNAs-Mediated Pyroptosis in Cerebral Ischemia-Reperfusion Injury: Pathophysiology, Mechanisms, and Therapeutic Perspectives.Current issues in molecular biology · 2025Review
- MicroRNAs regulating signaling pathways in cardiac fibrosis: potential role of the exercise training.American journal of physiology. Heart and circulatory physiology · 2024Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fibrotic remodelling contributes to heart failure in myocardial infarction. MicroRNAs (miRNAs) play a crucial role in myocardial fibrosis. However, current antifibrotic therapeutic strategies using miRNAs are far from effective. In this study, we aim to investigate the effect of miR-96-5p on cardiac fibrosis. Our work reveals a significant upregulation of miR-96-5p level in the ventricular tissues of myocardial infarction mice, as well as in neonatal rat cardiac fibroblasts stimulated with TGF-β or Ang II as shown by qPCR assay. In myocardial infarction mice,
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