Modulation of miR-10a-mediated TGF-β1/Smads signaling affects atrial fibrillation-induced cardiac fibrosis and cardiac fibroblast proliferation (Retracted article. See vol. 43, 2023)
Modulation of miR-10a-mediated TGF-β1/Smads signaling affects atrial fibrillation-induced cardiac fibrosis and cardiac fibroblast proliferation (Retracted article. See vol. 43, 2023)
复制标题
DOI：
10.1042/bsr20181931
复制
发表时间：
2019-02-28
影响因子：
4
通讯作者：
Yang, Bo
中科院分区：
文献类型：
--
作者：
Li, Peng-Fei;He, Rong-Hua;Yang, Bo
本研究采用大鼠心房颤动（AF）模型和miR-10a过表达或抑制的大鼠心脏成纤维细胞（CFs）研究miR-10a介导的转化生长因子β 1（TGF-β 1）/Smads信号通路在AF大鼠心脏纤维化和成纤维细胞增殖中的作用。结果显示，过表达miR-10a可显著延长AF持续时间，进一步升高胶原体积分数（CVF），并增加AF大鼠CFs的活力;这些结果与抑制miR-10a的大鼠形成对比（均P
Atrial fibrillation (AF) rat models and rat cardiac fibroblasts (CFs) with overexpressed or inhibited miR-10a were used to investigate the possible role of miR-10a-mediated transforming growth factor-beta (TGF-beta 1)/Smads signaling in cardiac fibrosis and fibroblast proliferation in rats with AF. Gene ontology and pathway enrichment analyses were used to identify the possible function of miR-10a in cardiac fibrosis. The results showed that overexpressed miR-10a significantly prolonged the duration of AF, further elevated the collagen volume fraction (CVF), and increased the viability of CFs in AF rats; these findings were in contrast with the findings for rats with inhibition of miR-10a (all P