[Endoplasmic reticulum stress in kidney diseases: a question of life and death?].
Increasing our understanding of the cellular and molecular mechanisms of acute and chronic kidney diseases will lead to the development of new biomarkers of early kidney injury and to the discovery of new therapeutic strategies to prevent the initiation of renal failure or to promote the renal regeneration after injury. The implication of the endoplasmic reticulum stress in kidney diseases is not well recognized, but increasing experimental evidences suggest its implication in a wide array of kidney insults. Beside its role in the regulation of cell death, the UPR response induced by the endoplasmic reticulum stress alters many cellular functions and constitutes an important mediator of inflammation and/or epithelial to mesenchymal transition. The purpose of this review is to summarize the existing data concerning the role of the endoplasmic reticulum stress during kidney injury and to clarify its precise role in chronic kidney disease.
Pallet
Nicolas
N
Inserm U775, centre universitaire des Saints-Pères, université Paris Descartes, 45, rue des Saints-Pères, 75006 Paris, France. nicolas.pallet@univ-paris5.fr
Bouvier
Nicolas
N
Beaune
Philippe
P
Legendre
Christophe
C
Thervet
Eric
E
Anglicheau
Dany
D
D002908:Chronic Disease; D004721:Endoplasmic Reticulum / Q000502:physiology*; D006801:Humans; D007668:Kidney / Q000098:blood supply; D007674:Kidney Diseases / Q000139:chemically induced / Q000209:etiology*; D007678:Kidney Glomerulus; D017510:Protein Folding; D015427:Reperfusion Injury / Q000209:etiology; D013312:Stress, Physiological