ArticleMolecular genetics and genomics : MGG2026
LncRNA CARD8-AS1 acts as a potential novel biomarker and promotes atrial fibrillation progression via the miR-31-5p/ARRB1 pathway.
Article in Molecular genetics and genomics : MGG, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAtrial fibrillation (AF) is a common arrhythmia linked to atrial fibrosis, yet reliable biomarkers and mechanisms remain unclear. LncRNAs have emerged as crucial regulators of cardiac remodelling and arrhythmogenesis, but the role of LncRNA CARD8-AS1 in AF has not been elucidated. This study aimed to investigate the expression, clinical diagnostic value, and molecular mechanism of CARD8-AS1 in AF.
methodsClinical data and serum samples were collected from 130 AF patients (76 with left atrial fibrosis, LAF) and 75 sinus rhythm (SR) individuals. RT-qPCR detected CARD8-AS1, miR-31-5p, and ARRB1 expression. ROC curves assessed diagnostic efficacy. In human atrial fibroblasts (HAFs), Ang-II was used to simulate fibrosis. CCK-8, Transwell, and molecular assays evaluated cell function and pathway molecules. Bioinformatics and luciferase assays verified molecular interactions.
resultsCARD8-AS1 was upregulated in AF patients, especially those with LAF, and effectively differentiated AF from SR and AF with LAF. CARD8-AS1 expression was correlated with LAd, LVEF, and fibrotic markers. In HAFs, Ang-II increased CARD8-AS1, enhancing cell viability, migration, and fibrotic marker expression, while CARD8-AS1 knockdown reversed these. CARD8-AS1 directly targeted miR-31-5p, which targeted ARRB1. The CARD8-AS1/miR-31-5p/ARRB1 axis mediated Ang-II-induced HAF activation.
conclusionsCARD8-AS1 is a potential diagnostic biomarker for AF and promotes AF progression via the miR-31-5p/ARRB1 pathway. Future studies may focus on validating the clinical utility of CARD8-AS1 in larger cohorts and exploring its therapeutic potential via targeted inhibition strategies.
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