PTEN inhibitor improves vascular remodeling and cardiac function after myocardial infarction through PI3k/Akt/VEGF signaling pathway.
PTEN inhibitor improves vascular remodeling and cardiac function after myocardial infarction through PI3k/Akt/VEGF signaling pathway.
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PTEN抑制剂通过PI3k/Akt/VEGF信号通路改善心肌梗死后血管重塑和心功能
DOI：
10.1186/s10020-020-00241-8
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发表时间：
2020-11-19
期刊：
影响因子：
--
通讯作者：
Qian X
中科院分区：
文献类型：
--
作者：
Feng Q;Li X;Qin X;Yu C;Jin Y;Qian X
心肌梗死(MI)是心血管疾病(CVD)死亡的主要原因。目前，心肌梗死的治疗效果仍不令人满意。因此，迫切需要开发一种新的治疗策略。结扎小鼠左前降支(LAD)造成心肌梗死。另一组小鼠在LAD结扎后1h静脉注射PTEN抑制剂BPV(1 mg/kg)，随后6d继续每日注射BPV。术后14天进行超声心动图检查。心肌梗死组小鼠PTEN表达增加，心功能受损，心肌细胞凋亡增加，血管生成减少。BPV治疗可明显改善心功能，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。PTEN抑制剂BPV能有效预防小鼠心肌梗死，突出了其作为候选治疗药物的潜力。
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. 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. 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. PTEN inhibitor BPV could effectively prevent myocardial infarction in mice, highlighting its potential as a candidate therapeutic drug.
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影响因子：
--
作者：
Jiang, Bing-Hua;Liu, Ling-Zhi
通讯作者：
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影响因子：
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作者：
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