PTEN inhibitor improves vascular remodeling and cardiac function after myocardial infarction through PI3k/Akt/VEGF signaling pathway

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. Ano...

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Bibliographic Details
Published in:Molecular medicine (Cambridge, Mass.) Mass.), 2020-11, Vol.26 (1), p.111-111, Article 111
Main Authors: Feng, Qiuting, Li, Xing, Qin, Xian, Yu, Cheng, Jin, Yan, Qian, Xiaojun
Format: Article
Language:English
Subjects:
Akt
Angiogenesis
Antibodies
Apoptosis
Cardiac function
Cardiomyocytes
Heart attacks
Ischemia
Ostomy
Phosphatase
PI3K
Proteins
PTEN inhibitor
Software
Surgery
Vascular endothelial growth factor
VEGF
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Summary: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.
ISSN:1076-1551
1528-3658
DOI:10.1186/s10020-020-00241-8