ArticleJournal of thoracic disease2020
DACT2 regulates structural and electrical atrial remodeling in atrial fibrillation.
Article in Journal of thoracic disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- TGF-β signalling drives chemotaxis of human induced pluripotent stem cell-derived cardiomyocytes in response to MI stimulus.Basic research in cardiology · 2026Article
- sVEGFR3 alleviates myocardial ischemia/reperfusion injury through regulating mitochondrial homeostasis and immune cell infiltration.Apoptosis : an international journal on programmed cell death · 2025Article
- Review
- Identification of candidate biomarkers and therapeutic agents for heart failure by bioinformatics analysis.BMC cardiovascular disorders · 2021Article
- WNT signaling in atrial fibrillation.Experimental biology and medicine (Maywood, N.J.) · 2021Review
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Authors and funding
12 authors.
Funding
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Abstract
backgroundAtrial fibrillation (AF) is the most common sustained arrhythmia. DACT2 is a novel and important mediator of signaling pathways. The aim of this study was to investigate the clinical significance and functions of DACT2 expression in AF.
methodsImmunohistochemistry was used to detect the DACT2 expression pattern in valvular disease patients. DACT2 was overexpressed in HL-1 cells and primary atrial fibroblasts. The expression levels of the potassium channel, the L-type calcium current channel, sodium ion channel proteins and collagen proteins were detected by real-time polymerase chain reaction (RT-PCR). The proteins involved in the Wnt and TGF-β signaling pathways were detected after DACT2 overexpression by western blotting.
resultsDACT2 expression was significantly associated with AF (P=0.016). The fibrosis ratio in the strong DACT2 expression group was significantly lower than that in the weak DACT2 expression group (weak: 0.198±0.091, strong: 0.129±0.064, P=0.048), and a negative correlation between DACT2 expression levels and fibrosis severity was observed (Spearman rho =-0.476, P=0.010). DACT2 significantly increased the expression levels of KCNE5 and decreased the levels of KCNH2 and SCN5A. Overexpression of DACT2 significantly inhibited the expression of collagen I and collagen III in primary rat atrial fibroblasts. DACT2 could facilitate β-catenin accumulation by reducing its phosphorylation at Thr41/Ser45 in HL-1 cells and inhibit the TGF-β signaling pathway in primary atrial fibroblasts.
conclusionsDACT2 played a role in AF by regulating both structural and electrical atrial remodeling and by affecting β-catenin accumulation and TGF-β signaling, and it could serve as a protective factor against AF in valvular heart disease.
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