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心力衰竭是许多器质性心脏疾病发展的终末阶段,其发病机制及病理生理过程复杂。传统的药物治疗虽然能有效缓解心力衰竭的症状,降低患者住院率,但其5年病死率仍超过50%[1]。随着分子生物学的发展及对心血管疾病发病机理认识的逐渐深入,基因治疗为心力衰竭提供了一种新的治疗途径。G蛋白偶联受体(G protein coupled receptors,GPCRs)是一类具有7个跨膜区蛋白的超家族。βAR是其之一,其可调节心脏对儿茶酚胺类物质的反应。βAR信号在一些心血管疾病中均下降。在心力衰蝎的进展过程中,βAR的密度和反
Heart failure is the terminal stage of the development of many organic heart diseases, and its pathogenesis and pathophysiological processes are complicated. Although the traditional drug therapy can effectively alleviate the symptoms of heart failure and reduce the hospitalization rate, but its 5-year mortality rate is still over 50% [1]. With the development of molecular biology and understanding of the pathogenesis of cardiovascular diseases, gene therapy provides a new therapeutic approach for heart failure. G protein coupled receptors (GPCRs) are a family of superfamilies with seven transmembrane proteins. βAR is one of them, which regulates the heart’s response to catecholamines. Beta AR signaling decreases in some cardiovascular diseases. In the progress of heart failure scorpion, the density and anti-βAR