Literature DB >> 19071081

[Endoplasmic reticulum stress in kidney diseases: a question of life and death?].

Nicolas Pallet1, Nicolas Bouvier, Philippe Beaune, Christophe Legendre, Eric Thervet, Dany Anglicheau.   

Abstract

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.

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Year:  2008        PMID: 19071081     DOI: 10.1016/j.nephro.2008.10.007

Source DB:  PubMed          Journal:  Nephrol Ther        ISSN: 1769-7255            Impact factor:   0.722


  2 in total

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Authors:  Pierre Galichon; Aurélien Bataille; Sophie Vandermeersch; Morgane Wetzstein; Yi-Chun Xu-Dubois; David Legouis; Alexandre Hertig; David Buob; Sandrine Placier; Naïke Bigé; Guillaume Lefevre; Chantal Jouanneau; Caroline Martin; Juan Lucio Iovanna; Eric Rondeau
Journal:  J Am Soc Nephrol       Date:  2016-07-22       Impact factor: 10.121

2.  Apelin promotes diabetic nephropathy by inducing podocyte dysfunction via inhibiting proteasome activities.

Authors:  Caixia Guo; Yu Liu; Wenjie Zhao; Shengnan Wei; Xiaoli Zhang; Wenying Wang; Xiangjun Zeng
Journal:  J Cell Mol Med       Date:  2015-06-23       Impact factor: 5.310

  2 in total

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