Why the study?
The study aimed to explore the potential role of the long non-coding RNA Dnm3os in the activation of cardiac fibroblasts.
Does silencing lncRNA Dnm3os prevent cardiac fibroblast activation in a TGF-β1-induced model?
Does silencing lncRNA Dnm3os prevent cardiac fibroblast activation in a TGF-β1-induced model?
Answers are grounded in this paper and cite their sources.
Silencing lncRNA Dnm3os may serve as a potential therapeutic target for cardiac fibrosis by inhibiting the TGF-β1/Smad2/3 signaling pathway.
cardiac fibroblast activation model induced by transforming growth factor-β1 (TGF-β1). Quantitative real-time polymerase chain reaction (RT-qPCR), Western blot, and collagen gel contraction test were used to identify the changes of activation phenotype and the expression of Dnm3os in cardiac fibroblasts. Small interfering RNA was used to silence Dnm3os to explore its role in the activation of cardiac fibroblasts. The results showed that the expression of Dnm3os was increased significantly in myocardial fibrotic tissues and in the activated cardiac fibroblasts. And the activation of cardiac fibroblasts could be alleviated by Dnm3os silencing. Furthermore, the TGF-β1/Smad2/3 pathway was activated during the process of cardiac fibroblasts activation, while was inhibited after silencing Dnm3os. The results suggest that Dnm3os silencing may affect the process of cardiac fibroblast activation by inhibiting TGF-β1/Smad2/3 signal pathway. Therefore, interfering with the expression of lncRNA Dnm3os may be a potential target for the treatment of cardiac fibrosis.
No takes yet. Share an insight, caveat, or question.
Kong et al. (2021) studied this question.
Synapse has enriched 8 closely related papers on similar clinical questions. Consider them for comparative context: