ArticleInternational journal of molecular medicine2018
MicroRNA-327 regulates cardiac hypertrophy and fibrosis induced by pressure overload.
Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Emerging roles of non-coding RNAs in fibroblast to myofibroblast transition and fibrotic diseases.Frontiers in pharmacology · 2024Review
- Noncoding RNAs: Master Regulator of Fibroblast to Myofibroblast Transition in Fibrosis.International journal of molecular sciences · 2023Review
- Mechanism of action of non-coding RNAs and traditional Chinese medicine in myocardial fibrosis: Focus on the TGF-β/Smad signaling pathway.Frontiers in pharmacology · 2023Review
- Activating transcription factor 3 inhibits angiotensin II‑induced cardiomyocyte viability and fibrosis by activating the transcription of cysteine‑rich angiogenic protein 61.Molecular medicine reports · 2022Article
- New Insights into the Functions of MicroRNAs in Cardiac Fibrosis: From Mechanisms to Therapeutic Strategies.Genes · 2022Review
- MicroRNA-451a attenuates angiotensin II-induced cardiac fibrosis and inflammation by directly targeting T-box1.Journal of physiology and biochemistry · 2022Article
- P21‑activated kinase 1 mediates angiotensin II‑induced differentiation of human atrial fibroblasts via the JNK/c‑Jun pathway.Molecular medicine reports · 2021Article
- Downregulated MicroRNA-327 Attenuates Oxidative Stress-Mediated Myocardial Ischemia Reperfusion Injury Through Regulating the FGF10/Akt/Nrf2 Signaling Pathway.Frontiers in pharmacology · 2021Article
- Targeting the renin-angiotensin-aldosterone system in fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2020Review
- microRNA Expression Profiles in Myocardium of High-Fat Diet-Induced Obesity Rat.Diabetes, metabolic syndrome and obesity : targets and therapy · 2020Article
- Deficiency of MicroRNA miR-1954 Promotes Cardiac Remodeling and Fibrosis.Journal of the American Heart Association · 2019Article
- The diagnostic value of circulating microRNAs in heart failure.Experimental and therapeutic medicine · 2019Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA (miRNA/miR) dysregulation has been reported to be fundamental in the development and progression of cardiac hypertrophy and fibrosis. In the present study, miR-327 levels in fibroblasts were increased in response to cardiac hypertrophy induced by transverse aortic constriction with prominent cardiac fibrosis, particularly when compared with the levels in unstressed cardiomyocytes. In neonatal rat cardiac fibroblasts, induced expression of miR-327 upregulated fibrosis-associated gene expression and activated angiotensin II-induced differentiation into myofibroblasts, as assessed via α-smooth muscle actin staining. By contrast, miR-327 knockdown mitigated angiotensin II-induced differentiation. Cardiac fibroblast proliferation was not affected under either condition. In a mouse model subjected to transverse aortic constriction, miR-327 knockdown through tail-vein injection reduced the development of cardiac fibrosis and ventricular dysfunction. miR-327 was demonstrated to target integrin β3 and diminish the activation of cardiac fibroblasts. Thus, the present study supports the use of miR-327 as a therapeutic target in the reduction of cardiac fibrosis.
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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.