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Knockdown circ_0040414 inhibits inflammation,apoptosis and promotes the proliferation of cardiomyocytes via miR-186-5p/PTEN/AKT axis in chronic heart failure
Authors:Yanling Feng  Biao Yan  Hongji Cheng  Jinlei Wu  Qinxiu Chen  Yuexing Duan  Peng Zhang  Dong Zheng  Guixiong Lin  Yufeng Zhuo
Institution:1. Department of Cardiology, Panyu District He Xian Memorial Hospital, Guangzhou, Guangdong, China;2. Department of Cardiovascular, Ningbo Yinzhou No.2 Hospital, Ningbo, Zhejiang, China
Abstract:Previous studies have shown that circ_0040414 is highly expressed in the blood of patients with heart failure (HF), which suggests that circ_0040414 is associated with heart failure (HF). However, the functional involvement of circ_0040414 in HF and its potential mechanism remains unclear. Consistent with previous studies, our study showed that the expression of circ_0040414 in the peripheral blood of patients with chronic heart failure (CHF) was significantly higher than that of healthy control, which indicated that circ_0040414 could be used as a diagnostic biomarker in patients with CHF. In cardiomyocytes, circ_0040414 increased the level of proapoptotic proteins Bax, cleaved-caspase 3 and reduced the expression of antiapoptotic protein Bcl-2. It also promoted inflammatory factors IL-6, TNF-α, and IL-β, but inhibited cell proliferation. In terms of mechanism, circ_0040414 upregulated the expression of phosphatase and tensin homolog (PTEN) through sponging miR-186-5p to inhibit AKT signaling activity. Our study uncovered a novel role and the mechanism of circ_0040414 in controlling CHF, enriched the molecular regulatory network in CHF, and may provide a possible strategy for the treatment of CHF.
Keywords:apoptosis  cardiomyocytes  Circ_0040414  inflammatory  proliferation
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