Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Wertheim cung cấp cho các bạn kiến thức về ngành y đề tài: VEGF attenuates development from cardiac hypertrophy to heart failure after aortic stenosis through mitochondrial mediated apoptosis and cardiomyocyte proliferation. | Xu et al. Journal of Cardiothoracic Surgery 2011 6 54 http content 6 1 54 JCTS JOURNAL OF CARDIOTHORACIC SURGERY RESEARCH ARTICLE Open Access VEGF attenuates development from cardiac hypertrophy to heart failure after aortic stenosis through mitochondrial mediated apoptosis and cardiomyocyte proliferation Xiao H Xuf Jing Xu1 Lei Xue1 Hai L Cao Xiang Liu and Yi J Chen Abstract Background Aortic stenosis AS affects 3 percent of persons older than 65 years and leads to greater morbidity and mortality than other cardiac valve diseases. Surgery with aortic valve replacement AVR for severe symptomatic AS is currently the only treatment option. Unfortunately in patients with poor ventricular function the mortality and long-term outcome is unsatisfied and only a minority of these patients could bear surgery. Our previous studies demonstrated that vascular endothelial growth factor VEGF protects cardiac function in myocardial infarction model through classic VEGF-PI3k-Akt and unclear mitochondrial anti-apoptosis pathways promoting cardiomyocyte CM proliferation as well. The present study was designed to test whether pre-operative treatment with VEGF improves AS-induced cardiac dysfunction to be better suitable for AVR and its potential mechanism. Methods Adult male mice were subjected to AS or sham operation. Two weeks later adenoviral VEGF Ad-VEGF enhanced green fluorescence protein Ad-EGFP as a parallel control or saline was injected into left ventricle free wall. Two weeks after delivery all mice were measured by echocardiography and harvested for further detection. Results AS for four weeks caused cardiac hypertrophy and left ventricular dysfunction. VEGF treatment increased capillary density protected mitochondrial function reduced CMs apoptosis promoted CMs proliferation and eventually preserved cardiac function. Conclusions Our findings indicate that VEGF could repair AS-induced transition from compensatory cardiac hypertrophy to heart .
