Fu Yongnan, Xiao Han, Zhang Youyi
Institute of Vascular Medicine, Peking University Third Hospital and Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, Beijing 100191, PR China.
Front Biosci (Elite Ed). 2012 Jan 1;4(5):1625-37. doi: 10.2741/484.
Beta-adrenoceptors (ARs), members of the G protein-coupled receptor (GPCR) superfamily, play a key role in the rapid regulation of myocardial function. Meanwhile, chronic catecholamine stimulation of adrenoceptors has been proved to be involved in the adverse myocardial remodeling, including cardiac hypertrophy, fibrosis, and apoptosis, which finally develop into heart failure. In the clinical situation, sympathetic hyperactivity is a key factor in the development of heart failure, and beta-blockers greatly improve the outcome of the disease. However, heart failure is still one of the leading causes of death. Therefore, a full understanding of the mechanism of beta-AR-mediated cardiac remodeling could indicate more targets for treating heart failure. This review summarizes a number of important signaling pathways involved in the process of cardiac pathological remodeling under chronic adrenergic stimulation.
β-肾上腺素能受体（ARs）是G蛋白偶联受体（GPCR）超家族的成员，在心肌功能的快速调节中起关键作用。同时，已证明肾上腺素能受体的慢性儿茶酚胺刺激参与不良心肌重塑，包括心脏肥大、纤维化和细胞凋亡，最终发展为心力衰竭。在临床情况下，交感神经过度活跃是心力衰竭发展的关键因素，β受体阻滞剂可大大改善疾病预后。然而，心力衰竭仍然是主要死因之一。因此，全面了解β-AR介导的心脏重塑机制可能为治疗心力衰竭指明更多靶点。本综述总结了慢性肾上腺素能刺激下参与心脏病理重塑过程的一些重要信号通路。
