PTEN公司
血管生成
医学
PI3K/AKT/mTOR通路
心肌梗塞
心功能曲线
蛋白激酶B
血管内皮生长因子
心脏病学
细胞凋亡
内科学
癌症研究
药理学
心力衰竭
生物
血管内皮生长因子受体
生物化学
作者
Qiuting Feng,Xing Li,Xian Qin,Changhong Yu,Yan Jin,Xiaojun Qian
标识
DOI:10.1186/s10020-020-00241-8
摘要
Abstract Background Myocardial infarction (MI) is the leading cause of death from cardiovascular disease (CVD). Currently, the efficacy for MI treatment remains unsatisfactory. Therefore, it is urgent to develop a novel therapeutic strategy. Methods Left anterior descending arteries (LAD) of mice were ligated to induce MI. Another set of mice were intravenously injected with PTEN inhibitor BPV (1 mg/kg) 1 h after LAD ligation and continued to receive BPV injection daily for the following 6 days. Mice were performed echocardiography 14 days after surgery. Results Mice in MI group displayed an increased expression of PTEN with impaired cardiac function, enhanced cardiomyocyte apoptosis and decreased angiogenesis. BPV treatment significantly improved cardiac function, with reduced cardiomyocyte apoptosis, promoted angiogenesis, and activated PI3K/Akt/vascular endothelial growth factor (VEGF) signaling pathway. Conclusion PTEN inhibitor BPV could effectively prevent myocardial infarction in mice, highlighting its potential as a candidate therapeutic drug.
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