心力衰竭β_3肾上腺素能受体与细胞凋亡的研究进展  

Progress in Heart Failure β_3-adrenergic Receptors and Apoptosis

作　　者：郑方方[1] 高海波[2] 孔一慧[1] 李为民[1] 

机构地区：[1]哈尔滨医科大学附属第一医院心内科 [2]哈尔滨工程大学医院内科,黑龙江哈尔滨150001

出　　处：《心血管病学进展》2013年第3期382-384,共3页Advances in Cardiovascular Diseases

基　　金：黑龙江省自然科学基金(D201121)

摘　　要：心力衰竭是许多心血管疾病发展到终末期的临床表现。心力衰竭发病机制除血流动力学异常,神经内分泌激活和心室重构外,细胞凋亡在衰竭心脏中的作用备受关注,凋亡使工作心肌细胞绝对数量减少,导致心肌收缩力下降。β肾上腺素能受体是调节心脏功能最有力的刺激物。心力衰竭时,β肾上腺素能受体信号转导通路的各个环节都发生改变,参与调节心肌舒张收缩功能、心室重塑和细胞凋亡。现将主要讨论心力衰竭、β3肾上腺素能受体与细胞凋亡的研究进展。Heart failure is the endstage clinical performance of many cardiovascular disease. The pathogenesis of heart failure in addi- tion to the hemodynamic abnormalities, neuroendocrine activation and ventricular remodeling, the role of apoptosis in the failing heart is atten- tioned, and apoptotic cells decrease in absolute number of the working myocardium,causing decreased myocardial contractility, β-adrenergic receptor is the most powerful stimulus for regulating heart function. Changes occurred in every link of the signal pathway regulated by β3-ad- renergic receptor during heart failure, which is involved in several aspects, such as the regulation of myocardial relaxation and contractile function, ventricle remodeling cell apoptosis and so on. This article focuses on research progress of heart failure, β3-adrenergic receptor and apoptosis.

关 键 词：心力衰竭 Β3肾上腺素能受体 细胞凋亡 

分 类 号：R541.61[医药卫生—心血管疾病]