ArticleJournal of the American Heart Association2019
Deficiency of MicroRNA miR-1954 Promotes Cardiac Remodeling and Fibrosis.
Article in Journal of the American Heart Association, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 27 citations in OpenAlex.
- Thrombospondin 1 aggravates cardiac remodeling in heart failure with preserved ejection fraction by inhibiting mitophagy.iScience · 2026Article
- Blocking TSP1 Ameliorates Diabetes Mellitus-Induced Erectile Dysfunction by Inhibiting the TGF-β/SMAD Pathway.The world journal of men's health · 2025Article
- Cardiac Fibroblasts: Helping or Hurting.Genes · 2025Review
- Epigenetic Regulation in Myocardial Fibroblasts and Its Impact on Cardiovascular Diseases.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Reviewing the Regulators of COL1A1.International journal of molecular sciences · 2023Review
- Article
- Novel Therapies for the Treatment of Cardiac Fibrosis Following Myocardial Infarction.Biomedicines · 2022Review
- Review
- MicroRNAs in cardiovascular diseases.Medical review (2021) · 2022Review
- MicroRNA-451a attenuates angiotensin II-induced cardiac fibrosis and inflammation by directly targeting T-box1.Journal of physiology and biochemistry · 2022Article
- Non-coding RNAs: Important participants in cardiac fibrosis.Frontiers in cardiovascular medicine · 2022Review
- Cardiac fibrosis.Cardiovascular research · 2021Review
- TGF-β and WNT signaling pathways in cardiac fibrosis: non-coding RNAs come into focus.Cell communication and signaling : CCS · 2020Review
- Deficiency of MicroRNA miR-1954 Promotes Cardiac Remodeling and Fibrosis.Journal of the American Heart Association · 2019Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background Cardiac fibrosis occurs because of disruption of the extracellular matrix network leading to myocardial dysfunction. Angiotensin II (AngII) has been implicated in the development of cardiac fibrosis. Recently, microRNAs have been identified as an attractive target for therapeutic intervention in cardiac pathologies; however, the underlying mechanism of microRNAs in cardiac fibrosis remains unclear. Next-generation sequencing analysis identified a novel characterized microRNA, miR-1954, that was significantly reduced in AngII-infused mice. The finding led us to hypothesize that deficiency of miR-1954 triggers cardiac fibrosis. Methods and Results A transgenic mouse was created using α-MHC (α-myosin heavy chain) promoter and was challenged with AngII infusion. AngII induced cardiac hypertrophy and remodeling. The in vivo overexpression of miR-1954 showed significant reduction in cardiac mass and blood pressure in AngII-infused mice. Further analysis showed significant reduction in cardiac fibrotic genes, hypertrophy marker genes, and an inflammatory gene and restoration of a calcium-regulated gene (Atp2a2 [ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 2]; also known as SERCA2), but no changes were observed in apoptotic genes. THBS1 (thrombospondin 1) is indicated as a target gene for miR-1954. Conclusions Our findings provide evidence, for the first time, that miR-1954 plays a critical role in cardiac fibrosis by targeting THBS1. We conclude that promoting the level of miR-1954 would be a promising strategy for the treatment of cardiac fibrosis.
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