PTEN 抑制剂通过 PI3k/Akt/VEGF 信号通路改善心肌梗死后的血管重构和心功能。
PTEN inhibitor improves vascular remodeling and cardiac function after myocardial infarction through PI3k/Akt/VEGF signaling pathway.
机构信息
Department of Cardiovascular, the Affiliated Wuxi No.2 People's Hospital of Nanjing Medical University, No.68, Zhongshan Road, Wuxi, 214002, Jiangsu, China.
Department of Respiratory, the Affiliated Wuxi No.2 People's Hospital of Nanjing Medical University, No.68, Zhongshan Road, Wuxi, 214002, Jiangsu, China.
出版信息
Mol Med. 2020 Nov 19;26(1):111. doi: 10.1186/s10020-020-00241-8.
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.
背景
心肌梗死（MI）是心血管疾病（CVD）导致死亡的主要原因。目前，MI 的治疗效果仍不尽人意。因此，迫切需要开发一种新的治疗策略。
方法
结扎小鼠的左前降支（LAD）以诱导 MI。另一组小鼠在 LAD 结扎后 1 小时静脉注射 PTEN 抑制剂 BPV（1mg/kg），并在接下来的 6 天内继续每天接受 BPV 注射。手术后 14 天对小鼠进行超声心动图检查。
结果
MI 组小鼠的 PTEN 表达增加，心脏功能受损，心肌细胞凋亡增强，血管生成减少。BPV 治疗可显著改善心脏功能，减少心肌细胞凋亡，促进血管生成，并激活 PI3K/Akt/血管内皮生长因子（VEGF）信号通路。
结论
PTEN 抑制剂 BPV 可有效预防小鼠心肌梗死，提示其可能成为候选治疗药物。
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