ArticleHeart and vessels2016
Rapid atrial pacing induces myocardial fibrosis by down-regulating Smad7 via microRNA-21 in rabbit.
Article in Heart and vessels, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.
- MicroRNAs in Atrial Fibrillation: from Expression Signatures to Functional Implications.Cardiovascular drugs and therapy · 2017Pooled it
- Epigenetics in Atrial Fibrillation: Molecular Mechanisms and Therapeutic Avenues.Reviews in cardiovascular medicine · 2026Review
- Dapagliflozin attenuates myocardial fibrosis after myocardial infarction through regulating Lnc-Ang362/miR-200b-3p.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- SMAD7: riding on fibrosis-limiting routes and beyond.EMBO molecular medicine · 2025Review
- TGF-β-Driven Atrial Fibrosis in Atrial Fibrillation: From Mechanistic Insights to Targeted Therapies.Aging and disease · 2025Review
- Animal and cellular models of atrial fibrillation: a review.Frontiers in cardiovascular medicine · 2025Review
- Interactions between atrial fibrosis and inflammation in atrial fibrillation.Frontiers in cardiovascular medicine · 2025Review
- Article
- Targeting inhibition of the inflammatory response: advances in the treatment of myocardial fibrosis with natural medicine and active ingredients.Frontiers in cardiovascular medicine · 2025Review
- MicroRNAs regulating signaling pathways in cardiac fibrosis: potential role of the exercise training.American journal of physiology. Heart and circulatory physiology · 2024Review
- Atrial fibrillation in human patients is associated with increased collagen type V and TGFbeta1.International journal of cardiology. Heart & vasculature · 2024Article
- Non-coding RNA and arrhythmias: expression, function, and molecular mechanism.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2023Review
- microRNAs as Biomarkers of Endothelial Dysfunction and Therapeutic Target in the Pathogenesis of Atrial Fibrillation.International journal of molecular sciences · 2023Review
- Post-Transcriptional Regulation of Molecular Determinants during Cardiogenesis.International journal of molecular sciences · 2022Review
- Myocardial fibrosis in congenital heart disease.Frontiers in pediatrics · 2022Review
- MiR-208b/miR-21 Promotes the Progression of Cardiac Fibrosis Through the Activation of the TGF-β1/Smad-3 Signaling Pathway: AnFrontiers in cardiovascular medicine · 2022Article
- Circulatory MicroRNAs in Plasma and Atrial Fibrillation in the General Population: The Rotterdam Study.Genes · 2021Article
- Biomarkers in the clinical management of patients with atrial fibrillation and heart failure.Journal of geriatric cardiology : JGC · 2021Article
- A narrative review of non-coding RNAs in atrial fibrillation: potential therapeutic targets and molecular mechanisms.Annals of translational medicine · 2021Review
- Integrative analysis reveals essential mRNA, long non-coding RNA (lncRNA), and circular RNA (circRNA) in paroxysmal and persistent atrial fibrillation patients.Anatolian journal of cardiology · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tachycardia-induced atrial fibrosis is a hallmark of the structural remodeling of atrial fibrillation (AF). The mechanisms underlying tachycardia-induced atrial fibrosis remain unclear. In our previous study, we found that Smad7-downregulation promoted the development of atrial fibrosis in AF. Fibroblasts are enriched in microRNA-21 (miR-21), which contributes to the development of fibrosis and heart failure in the cardiovascular system. Our study was designed to test the hypothesis that miR-21 reinforces the TGF-β1/Smad signaling pathway in AF-induced atrial fibrosis by down-regulating Smad7. Rapid atrial pacing (RAP, 1000 ppm) was applied to the left atrium of the rabbit heart to induce atrial fibrillation and fibrosis. qRT-PCR and northern blot analysis revealed that RAP caused a marked increase in the expression of miR-21. Transfection with a miR-21 inhibitor significantly increased the expression of Smad7, while the expression of collagen I/III significantly decreased. These changes were implicated in the AF-induced release of miR-21 and down-regulation of Smad7. Adult rat cardiac fibroblasts treated with TGF-β1 showed increased miR-21 expression and decreased Smad7 expression. Pretreatment with a TGF-β1 inhibitor reduced the TGF-β1-induced up-regulation of miR-21. Pretreatment with pre-miR-21 and a miR-21 inhibitor significantly decreased and increased Smad7 expression, respectively. This result was negatively correlated with the expression of collagen I/III in fibroblasts. Moreover, the results of a luciferase activity assay suggest that Smad7 is a validated miR-21 target in CFs. Our results provide compelling evidence that the miR-21 specific degradation of Smad7 may decrease the inhibitory feedback regulation of TGF-β1/Smad signaling and serves as a new insight of the mechanism of atrial fibrosis in atrial fibrillation.
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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.