心力衰竭中内质网应激相关诱导因子的研究进展

Research Progress in Endoplasmic Reticulum Stress Inducer in Heart Failure

内质网合成及加工蛋白的功能异常可引起未折叠蛋白的聚集,从而引起内质网应激(ERS)和未折叠蛋白反应。适度的ERS使心肌细胞发生代偿性肥大,但过强和持续的ERS可使心肌细胞由代偿转向凋亡,从而致心力衰竭。该文综述了各种ERS诱导因子在心力衰竭发生、发展中的作用,阐明ERS在心力衰竭病理形成过程中发挥着重要的作用,也为心力衰竭的治疗开启了新思路。

The dysregulatiou of protein synthesis/processing in the endoplasmic reticulum can cause the accumulation of unfolded proteins,leading to endoplasmic reticulum stress （ ERS ） and the activation of the unfolded protein response. Although cardiac hypertrophy may be initially adaptive, prolonged or severe endoplasmic reticulum stress resulting from the increased protein synthesis associated with cardiac hypertrophy can lead to apoptosis of myocardium and result in chronic heart failure. This review focuses on ERS inducers function in the occurrence and development of heart failure, clarifying ERS important role in the pathological process of heart failure, and providing a new treatment for heart failure.