ArticleJournal of inflammation research2020
MicroRNA-21 Mediates a Positive Feedback on Angiotensin II-Induced Myofibroblast Transformation.
Article in Journal of inflammation research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Unifying and unique roles of non-coding RNA biomarkers in liver and heart fibrosis.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2026Review
- Article
- Cardiovascular toxicity induced by immune checkpoint inhibitors: mechanisms linking immune dysregulation and myocardial fibrosis.American journal of clinical and experimental immunology · 2026Review
- Exosomal miRNAs: A New Frontier in Cardiovascular Disease Diagnosis and Treatment.Journal of cardiovascular translational research · 2025Review
- MicroRNA Signatures in Cardiometabolic Disorders as a Next-Generation Diagnostic Approach: Current Insight.International journal of molecular sciences · 2025Review
- Targeting inhibition of the inflammatory response: advances in the treatment of myocardial fibrosis with natural medicine and active ingredients.Frontiers in cardiovascular medicine · 2025Review
- The Effects of MicroRNAs in the Development of Heart Failure.Current cardiology reports · 2023Review
- 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
- Molecular mechanisms of isoflavone puerarin against cardiovascular diseases: What we know and where we go.Chinese herbal medicines · 2022Review
- CTRP3 alleviates cardiac ischemia/reperfusion injury via LAMP1/JIP2/JNK signaling pathway.Aging · 2022Article
- Superhydrophilic PLGA-Graft-PVP/PC Nanofiber Membranes for the Prevention of Epidural Adhesion.International journal of nanomedicine · 2022Article
- Exosome-Mediated miR-21 Was Involved in the Promotion of Structural and Functional Recovery Effect Produced by Electroacupuncture in Sciatic Nerve Injury.Oxidative medicine and cellular longevity · 2022Article
- The Networks of Noncoding RNAs and Their Direct Molecular Targets in Myocardial Infarction.International journal of biological sciences · 2022Review
- Exercise Training Alleviates Cardiac Fibrosis through Increasing Fibroblast Growth Factor 21 and Regulating TGF-β1-Smad2/3-MMP2/9 Signaling in Mice with Myocardial Infarction.International journal of molecular sciences · 2021Article
- Mesenchymal Stem Cells Therapies on Fibrotic Heart Diseases.International journal of molecular sciences · 2021Review
- Positive feedback regulation between USP15 and ERK2 inhibits osteoarthritis progression through TGF-β/SMAD2 signaling.Arthritis research & therapy · 2021Article
- miR-21 in Human Cardiomyopathies.Frontiers in cardiovascular medicine · 2021Review
- MiR-21-3p Inhibits Adipose Browning by Targeting FGFR1 and Aggravates Atrial Fibrosis in Diabetes.Oxidative medicine and cellular longevity · 2021Article
- Inhibitory effect of microRNA-21 on pathways and mechanisms involved in cardiac fibrosis development.Therapeutic advances in cardiovascular diseaseReview
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivePost myocardial infarction (MI) fibrosis has been identified as an important factor in the progression of heart failure. Previous studies have revealed that microRNA-21 (miR-21) plays an important role in the pathogenesis of fibrosis. The purpose of this study was to explore the role of miR-21 in post-MI cardiac fibrosis. MATERIAL AND
methodsMI was established in wild-type (WT) and miR-21 knockout (KO) mice. Primary mice cardiac fibroblasts (CFs) were isolated from WT and miR-21 KO mice and were treated with angiotensin II (Ang II) or Sprouty1 (Spry1) siRNA. Histological analysis and echocardiography were used to determine the extent of fibrosis and cardiac function.
resultsCompared with WT mice, miR-21 KO mice displayed smaller fibrotic areas and decreased expression of fibrotic markers and inflammatory cytokines. In parallel, Ang II-induced myofibroblasts transformation was partially inhibited upon miR-21 KO in primary CFs. Mechanistically, we found that the expression of Spry1, a previously reported target of miR-21, was markedly increased in miR-21 KO mice post MI, further inhibiting ERK1/2 activation. In vitro studies showed that Ang II activated ERK1/2/TGF-β/Smad2/3 pathway. Phosphorylated Smad2/3 further enhanced the expression of α-SMA and FAP and may promote the maturation of miR-21, thereby downregulating Spry1. Additionally, these effects of miR-21 KO on fibrosis were reversed by siRNA-mediated knockdown of Spry1.
conclusionOur findings suggest that miR-21 promotes post-MI fibrosis by targeting Spry1. Furthermore, it mediates a positive feedback on Ang II, thereby inducing the ERK/TGF-β/Smad pathway. Therefore, targeting the miR-21-Spry1 axis may be a promising therapeutic option for ameliorating post-MI cardiac fibrosis.
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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.