PTEN inhibitor improves vascular remodeling and cardiac function after myocardial infarction through PI3k/Akt/VEGF signa
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(2020) 26:111 Feng et al. Mol Med https://doi.org/10.1186/s10020-020-00241-8
Open Access
RESEARCH ARTICLE
PTEN inhibitor improves vascular remodeling and cardiac function after myocardial infarction through PI3k/Akt/VEGF signaling pathway Qiuting Feng1†, Xing Li1†, Xian Qin1, Cheng Yu1, Yan Jin1 and Xiaojun Qian2*
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. Keywords: PTEN inhibitor, Angiogenesis, Cardiac function, PI3K, Akt, VEGF, Apoptosis Background Acute myocardial infarction (AMI) occurs when blood flow dramatically decreases or suddenly stops, which causes acute and persistent ischemia and hypoxia of coronary arteries, leading to severe impairment of cardiac function (Boateng and Sanborn 2013). Myocardial infarction (MI) is the leading cause of death from cardiovascular disease (CVD), which is the number one cause of death worldwide (Saleh and Ambrose 2018). Many *Correspondence: [email protected] † Qiuting Feng and Xing Li have contributed equally to this work 2 Department of Respiratory, the Affiliated Wuxi No.2 People’s Hospital of Nanjing Medical University, No.68, Zhongshan Road, Wuxi 214002, Jiangsu, China Full list of author information is available at the end of the article
cardiomyocytes necrosis in the infarcted hearts are eventually replaced by fibrous tissue, resulting in the loss of cardiac function (Bahit et al. 2018). According to the report of World Health Organization (WHO), there are 32.4 million myocardial infarctions globally every year. In addition, patients who underwent previous MI are at the highest risk for further coronary and cerebral events (Lu et al. 2015). Similarly, survivors from MI are more susceptible of recurrent infarctions (Schumacher et al. 1998). In fact, MI is an imbalance between blood supply in coronary and myocardial demand (Reddy et al. 2015; Ibanez et al. 2018). Currently, the most effectively therapeutic approach for MI is still percutaneous coronary intervention (PCI) and most medications for MI, including aspirin, thrombolytics, vasodila
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