Key result
MiR-324-3p expression was significantly decreased in patients with atrial fibrillation, and its overexpression inhibited cardiac fibroblast proliferation by targeting TGF-β1.
Why the study?
Whether miR-324-3p is involved in myocardial fibrosis in AF and its molecular mechanisms in regulating cardiac fibroblasts remain unknown.
p-value: p=<0.01
miR-324-3p is downregulated in atrial fibrillation and its overexpression inhibits cardiac fibroblast proliferation by targeting TGF-β1, highlighting a potential therapeutic target for AF-related myocardial fibrosis.
Lower miR-324-3p in AF was associated with fibroblast proliferation; leaves open miRNA-based antifibrotic strategies for prospective trials.
Atrial fibrillation (AF), one of the common clinical arrhythmias, lacks effective treatment manners. Cardiac fibroblasts play an essential role in myocardial fibrosis and cardiac remodeling, which are involved in AF progression. Reportedly, MicroRNAs (miRNAs) regulate the myocardial fibrosis in AF. However, whether miR-324-3p involves myocardial fibrosis in AF and the tentative molecular mechanisms of miR-324-3p regulating cardiac fibroblasts during AF remains unknown. In the present study, miR-324-3p was found to be decreased in patients with AF and AF rat model. Next, we investigated the effect of miR-324-3p on myocardial fibroblast proliferation through miR-324-3p overexpression and found that miR-324-3p inhibited fibroblast proliferation in vitro. Furthermore, we found that miR-324-3p directly targeted transforming growth factor β1 in fibroblast, which may be involved in the development of myocardial fibrosis during AF. Meanwhile, miR-324-3p mimics treatment suppressed the PI3K/AKT signaling pathway in fibroblast. These results demonstrated a molecular mechanism of miR-324-3p regulating fibroblast proliferation in vitro, which might provide a novel potential treatment manner in AF in clinic.
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Xu et al. (2020) studied Atrial Fibrillation (n=40). miR-324-3p vs. Healthy controls was evaluated on miR-324-3p expression levels (p=<0.01). MiR-324-3p expression was significantly decreased in patients with atrial fibrillation, and its overexpression inhibited cardiac fibroblast proliferation by targeting TGF-β1.
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