Kitamura Masanori
Department of Molecular Signaling, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Shimokato 1110, Yamanashi, Japan.
Am J Physiol Renal Physiol. 2008 Aug;295(2):F323-34. doi: 10.1152/ajprenal.00050.2008. Epub 2008 Mar 26.
A number of pathophysiological insults lead to accumulation of unfolded proteins in the endoplasmic reticulum (ER) and cause ER stress. In response to accumulation of unfolded/misfolded proteins, cells adapt themselves to the stress condition via the unfolded protein response (UPR). For the cells, UPR is a double-edged sword. It triggers both prosurvival and proapoptotic signals. ER stress and UPR may, therefore, be involved in a diverse range of pathological situations. However, currently, information is limited regarding roles of ER stress and UPR in the renal pathophysiology. This review describes current knowledge on the relationship between ER stress and diseases and summarizes evidence for the link between ER stress/UPR and renal diseases.
多种病理生理损伤会导致内质网(ER)中未折叠蛋白的积累,并引发内质网应激。作为对未折叠/错误折叠蛋白积累的反应,细胞通过未折叠蛋白反应(UPR)来适应应激状态。对细胞而言,UPR是一把双刃剑。它既触发促生存信号,也触发促凋亡信号。因此,内质网应激和UPR可能参与多种病理情况。然而,目前关于内质网应激和UPR在肾脏病理生理学中的作用的信息有限。本综述描述了关于内质网应激与疾病之间关系的现有知识,并总结了内质网应激/UPR与肾脏疾病之间联系的证据。