ArticleCardiovascular diagnosis and therapy2025
LncRNA-5829: a novel inhibitor of cardiac fibrosis.
Article in Cardiovascular diagnosis and therapy, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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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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1 citing paper in PubMed.
- Transcriptomic Remodeling of Pulmonary Vein Sleeves Suggests a Role in Atrial Arrhythmogenesis in Thoroughbred Horses.Annals of the New York Academy of Sciences · 2026Article
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9 authors.
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Abstract
Background: Recent studies have proved that long non-coding RNAs (lncRNAs) are closely related to the pathogenesis of cardiovascular diseases (CVDs), but their exact regulatory mechanism including non-coding as well as coding function in myocardial fibrosis need to be further explored. This study aims to explore the role of a novel and highly conserved lncRNA-5829 in myocardial fibrosis. Methods: Thirty-two male C57BL/6 mice weighing 20-25 g (8 weeks old) were cultured under specific pathogen-free (SPF) conditions prior to the start of the experiment. Myocardial fibrosis cells and mouse models were established by transforming growth factor-β1 (TGF-β1) induction and ligation of the left anterior descending coronary artery (LAD) surgery. After cell overexpression or knockdown of lncRNA-5829, the levels of myocardial fibrosis markers, cell proliferation, cell viability, and α smooth muscle actin (α-SMA) were measured by real-time polymerase chain reaction (PCR), Western blot and 5-ethynyl-2'-deoxyuridine (EdU) staining, cell counting kit-8 (CCK-8), immunofluorescence technique, respectively. After mouse tail vein injection of lncRNA-5829 overexpression plasmid, the levels of myocardial fibrosis markers, cardiac function, myocardial collagen distribution, and myocardial injury were measured by real-time PCR, Western blot, and echocardiography, Masson staining, and hematoxylin-eosin staining (HE staining), respectively. Furthermore, the localization of lncRNA-5829 in cardiac fibroblasts was observed by the fluorescent in situ hybridization (FISH) assay. Results: The expression of lncRNA-5829 is downregulated in myocardial fibrosis. Conclusions: This study demonstrated that lncRNA-5829, as a new anti-fibrotic factor, may play an important role in regulating the pathological process of myocardial fibrosis, and is a potential molecular target for the treatment of cardiac fibrosis and related heart diseases.
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