内质网应激在肺动脉高压发病机制中的研究进展

Study advances of endoplasmic reticulum stress in the pathogenesis of pulmonary arterial hypertension

肺动脉高压指肺动脉压力升高超过一定界值的一种血流动力学和病理生理状态,由于肺微血管结构重塑,导致肺血管阻力增加,压力值升高,最终引起右心室衰竭和死亡,但其发生的分子机制尚不清楚。近年来,研究表明内质网应激可能在肺动脉高压的发病机制中起关键作用。本文就内质网应激在肺动脉高压中的作用进行综述,首先回顾内质网应激后未折叠蛋白反应的机制,介绍内质网应激对不同血管细胞的影响,最后讨论减轻内质网应激对肺动脉高压的治疗作用,以期为肺动脉高压的治疗带来新的方向。

Pulmonary arterial hypertension(PAH)refers to a hemodynamic and pathophysiological state in which pulmonary pressure is elevated above a certain threshold,resulting in increased pulmonary vascular resistance and elevated pressure values due to remodeling of pulmonary microvascular structures,which eventually causes right ventricular failure and death,but the molecular mechanism of its occurrence is still unclear.In recent years,studies have suggested that endoplasmic reticulum stress(ERS)may play a key role in the pathogenesis of PAH.This paper reviews the role of ERS in PAH.Firstly,it reviews the mechanism of unfolded protein response after ERS,then introduces the impacts of ERS on different vascular cells,and finally discusses the therapeutic effect of reducing ERS on PAH,which is expected to provide a new study direction for the treatment of PAH.