甲状旁腺激素在心肌肥厚和纤维化中的作用机制  

Role and Mechanism of Parathyroid Hormone in Myocardial Hypertrophy and Fibrosis

作　　者：黄仕琼 李利华 HUANG Shiqiong;LI Lihua(Department of Gerontology,the First Affiliated Hospital of Dali University,Dali 671000,China)

机构地区：[1]大理大学第一附属医院老年病科,云南大理671000

出　　处：《医学综述》2022年第10期1879-1884,共6页Medical Recapitulate

基　　金：国家自然科学基金(81860084)。

摘　　要：心力衰竭是各种心血管疾病的终末阶段,有较高的病死率和再入院率。病理性心肌肥厚和心肌纤维化是心力衰竭发病的病理生理学基础。甲状旁腺激素可通过调节心肌细胞钙代谢、肾素-血管紧张素-醛固酮系统活性、成纤维细胞生长因子-23分泌,激活促分裂原活化的蛋白激酶通路等途径,导致心肌肌纤维紊乱、胶原蛋白/成纤维细胞增殖,从而引起心肌肥厚和纤维化的发生。明确甲状旁腺激素在心肌肥厚和纤维化中的可能机制,可为心力衰竭的治疗提供新的干预靶点。Heart failure is the final stage of various cardiovascular diseases,with a high mortality and readmission rate.Pathological myocardial hypertrophy and myocardial fibrosis are the pathophysiological basis of heart failure.The parathyroid hormone can lead to myocardial fiber disorder and collagen/fibroblast proliferation,resulting in myocardial hypertrophy and fibrosis via regulating calcium,the renin-angiotensin-aldosterone system,and fibroblast growth factor-23,and mitogen-activated protein kinase pathway.Understanding the possible mechanism of parathyroid hormone in myocardial hypertrophy and fibrosis can provide a new intervention target for the treatment of heart failure.

关 键 词：心肌肥厚 心肌纤维化 心力衰竭 甲状旁腺激素 肾素-血管紧张素-醛固酮系统 

分 类 号：R541[医药卫生—心血管疾病]