内质网应激机制与心力衰竭  

Endoplasmic Reticulum Stress and Heart Failure

作　　者：夏珍[1] 李菊香[1] 

机构地区：[1]南昌大学第二附属医院心内科,中国南昌330006

出　　处：《国际老年医学杂志》2014年第2期80-83,87,共5页International Journal of Geriatrics

基　　金：国家自然基金（81060013）

摘　　要：内质网是细胞中蛋白质翻译合成的场所，是细胞内的钙库，调节细胞应激反应，维持细胞内稳态。适当程度的内质网应激尚能保护细胞避免损伤，而过度应激时，保护机制不能与损伤相抗衡，则会激活凋亡信号通路而导致细胞凋亡。心力衰竭是心血管疾病晚期共有的器官损害，其病理生理基础是细胞凋亡。内质网应激参与心力衰竭的发生发展，干预内质网应激可能成为心力衰竭治疗的新靶点。The endoplasmic reticulum is the place of protein synthesis and the calcium stores in the cell, which can regulate stress reaction of cell and maintain intracellular homeostasis. Appropriative levels of endoplasmic reticulum stress can still protect cells from injury. However, excessive stress cannot make the protection mechanism contend with the injury, and apoptotic signaling path- ways which lead to cell apoptosis will he activated. Heart failure is a common advanced organ damage of cardiovascular diseases and cell apoptosis is the pathophysiologic basis. Endoplasmic reticulum stress involves in the origination and development of heart failure. Therefor, intervention of endoplasmic reticulum stress may provide a new target for treating heart failure.

关 键 词：内质网应激 细胞凋亡 心力衰竭 

分 类 号：R363.27[医药卫生—病理学]