Endoplasmic reticulum stress and kidney dysfunction. (1st August 2018)

• Record Type: Journal Article
• Authors: Gallazzini, Morgan; Pallet, Nicolas
• Is Part Of: Biology of the cell. Volume 110:Number 9(2018)
• Page Start: 205
• Page End: 216
• Publication Date: 2018-08-01
• Subjects: acute kidney injury -- chronic kidney disease -- endoplasmic reticulum stress -- proteinuria -- unfolded protein response; Cytology -- Periodicals; Electron microscopy -- Periodicals; 571.6
• DOI: 10.1111/boc.201800019
• Languages: English
• ISSNs: 0248-4900

Abstract

Abstract: Chronic kidney disease (CKD) affects millions of persons worldwide and constitutes a major public health problem. Therefore, understanding the molecular basis of CKD is a key challenge for the development of preventive and therapeutic strategies. A major contributor to chronic histological damage associated with CKD is acute kidney injury (AKI). At the cellular level, kidney injuries are associated with microenvironmental alterations, forcing cells to activate adaptive biological processes that eliminate the stressor and generate alarm signals. These signalling pathways actively participate in tissue remodelling by promoting inflammation and fibrogenesis, ultimately leading to CKD. Many stresses that are encountered upon kidney injury are prone to trigger endoplasmic reticulum (ER) stress. In the kidney, ER stress both participates in acute and chronic histological damages, but also promotes cellular adaptation and nephroprotection. In this review, we will discuss the implication of ER stress in the pathophysiology of AKI and CKD progression, and we will give a critical analysis of the current experimental and clinical evidence that support ER stress as a mediator of kidney damage. Abstract : Review : Impact of the ER stress response upon acute and chronic kidney injuries. The UPR is activated in response to acute kidney injury (AKI), and in general, protects against the deleterious effect of ER stress in the short term. However, ER stress could be involved in the transition to chronic kidney disease in driving inadequate tissue remodelling, leading to chronic structural deterioration. In turn, ER stress triggered by proteinuria and chronic ischemia (induced by fibrosis and capillary rarefaction) fosters tissue remodelling and chronic kidney disease progression. .