ArticleHuman cell2018
Atrial overexpression of microRNA-27b attenuates angiotensin II-induced atrial fibrosis and fibrillation by targeting ALK5.
Article in Human cell, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 56 citations in OpenAlex.
- MicroRNAs in Pediatric Primary Hypertension: Promising Biomarkers or Context-Dependent Regulators?-A Narrative Review.Biomolecules · 2026Review
- TGF-β-Driven Atrial Fibrosis in Atrial Fibrillation: From Mechanistic Insights to Targeted Therapies.Aging and disease · 2025Review
- Interactions between atrial fibrosis and inflammation in atrial fibrillation.Frontiers in cardiovascular medicine · 2025Review
- Comprehensive Analysis of Immune Cell Infiltration and M2-Like Macrophage Biomarker Expression Patterns in Atrial Fibrillation.International journal of general medicine · 2024Article
- MicroRNA-499-5p inhibits transforming growth factor-β1-induced Smad2 signaling pathway and suppresses fibroblast proliferation and collagen synthesis in rat by targeting TGFβ-R1.Molecular biology reports · 2023Article
- Article
- microRNAs as Biomarkers of Endothelial Dysfunction and Therapeutic Target in the Pathogenesis of Atrial Fibrillation.International journal of molecular sciences · 2023Review
- Noncoding RNAs and Cardiac Fibrosis.Reviews in cardiovascular medicine · 2023Review
- Research progress of non-coding RNA in atrial fibrillation.Frontiers in cardiovascular medicine · 2023Review
- Article
- New Insights into the Functions of MicroRNAs in Cardiac Fibrosis: From Mechanisms to Therapeutic Strategies.Genes · 2022Review
- MicroRNAs in cardiovascular diseases.Medical review (2021) · 2022Review
- Post-Transcriptional Regulation of Molecular Determinants during Cardiogenesis.International journal of molecular sciences · 2022Review
- Research Progress of Myocardial Fibrosis and Atrial Fibrillation.Frontiers in cardiovascular medicine · 2022Review
- Focusing on Mechanoregulation Axis in Fibrosis: Sensing, Transduction and Effecting.Frontiers in molecular biosciences · 2022Review
- miR-455-5p regulates atrial fibrillation by targeting suppressor of cytokines signaling 3.Journal of physiology and biochemistry · 2021Article
- 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
- Transcriptome analysis reveals key pathways that vary in patients with paroxysmal and persistent atrial fibrillation.Experimental and therapeutic medicine · 2021Article
- Atrial fibrosis underlying atrial fibrillation (Review).International journal of molecular medicine · 2021Article
- A Comprehensive miRNome Analysis of Macrophages Isolated from db/db Mice and Selected miRNAs Involved in Metabolic Syndrome-Associated Cardiac Remodeling.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Atrial fibrosis influences atrial fibrillation (AF) development by transforming growth factor beta 1 (TGF-β1)/Smad pathway. Although microRNAs are implicated in the pathogenesis of various diseases, information regarding the functional role of microRNAs in atrial dysfunction is limited. In the present study, we found that microRNA-27b (miR-27b) was the dominant member of miR-27 family expressed in left atrium. Moreover, the expression of miR-27b was significantly reduced after angiotensin II (AngII) infusion. Masson's trichrome staining revealed that delivery of miR-27b adeno-associated virus to left atrium led to a decrease in atrial fibrosis induced by AngII. The increased expression of collagen I, collagen III, plasminogen activator inhibitor type 1 and alpha smooth muscle actin was also inhibited after miR-27b upregulation. In isolated perfused hearts, miR-27b restoration markedly attenuated AngII-induced increase in interatrial conduction time, AF incidence and AF duration. Furthermore, our data evidence that miR-27b is a novel miRNA that targets ALK5, a receptor of TGF-β1, through binding to the 3' untranslated region of ALK5 mRNA. Ectopic miR-27b suppressed luciferase activity and expression of ALK5, whereas inhibition of miR-27b increased ALK5 luciferase activity and expression. Additionally, miR-27b inhibited AngII-induced Smad-2/3 phosphorylation without altering Smad-1 activity. Taken together, our study demonstrates that miR-27b ameliorates atrial fibrosis and AF through inactivation of Smad-2/3 pathway by targeting ALK5, suggesting miR-27b may play an anti-fibrotic role in left atrium and function as a novel therapeutic target for the treatment of cardiac dysfunction.
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