Endoplasmic reticulum stress as a progression factor for kidney injury.
Dysfunction of endoplasmic reticulum (ER) maintaining protein homeostasis can result from various disturbances, including hypoxia or oxidative stress, which lead to an imbalance between protein-folding capacity and protein-folding load. This in turn leads to ER stress and induction of the unfolded protein response (UPR). The UPR initially serves as an adaptive response, but also induces apoptosis in cells under severe or prolonged ER stress. Accumulating evidence indicates that ER stress contributes to glomerular and tubular damages in kidney disease. These findings emphasize the importance of ER stress as a new progression factor and the interesting future possibility of renoprotective strategies targeting ER stress. These therapeutic approaches may act by breaking the vicious cycle of oxidative stress, hypoxia, and ER stress.
Inagi
Reiko
R
Division of Nephrology and Endocrinology, University of Tokyo School of Medicine, 7-3-1 Hongo Bunkyo-ku, Tokyo 113-8655, Japan.
D000818:Animals; D001343:Autophagy / Q000502:physiology; D016923:Cell Death / Q000502:physiology; D002470:Cell Survival / Q000502:physiology; D018450:Disease Progression; D016503:Drug Delivery Systems / Q000379:methods*; D004721:Endoplasmic Reticulum / Q000378:metabolism* / Q000502:physiology; D006801:Humans; D007674:Kidney Diseases / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology; D013312:Stress, Physiological / Q000502:physiology*; D056811:Unfolded Protein Response / Q000502:physiology*