内质网应激与膜性肾病

Endoplasmic reticulum stress and membranous nephropathy

内质网(endoplasmic reticulum,ER)是调节蛋白质合成、折叠及组装的重要场所。各种原因如ER中Ca2+缺乏均可引起ER功能紊乱,使蛋白质从ER向高尔基体的转运受阻[1],最终引发内质网应激(endoplasmic reticulum stress,ERS)。细胞通过激活未折叠蛋白反应(the unfolded protein response,UPR)保护ERS引起损伤的细胞,强烈或持久的ERS又可启动UPR的促凋亡信号。肾病尤其是膜性肾病(membranous nephropathy,MN)的发生发展与ERS密切相关,文中主要阐述ERS在MN发病机制中的作用。

Endoplasmic reticulum(ER) is an intracellular compartment that plays a critical role in the processing,folding and assembling of newly synthesized proteins.A stress-induced impairment of ER membrane integrity can be injurious by causing leakage of calcium ions and other ER luminal components and interfering with protein transport to Golgi apparatus.This in turn initiates the unfolded protein response(UPR),an integrated intracellular signaling pathway that responds to ER stress.As a defense mechanism,UPR can protect the cells from being impaired by ER stress.Also,UPR can activate pathways of cell death in response to prolonged or severe ER stress.This review highlights the current knowledge of ER stress in membranous nephropathy.