Endoplasmic reticulum stress and kidney dysfunction

被引:54
作者
Gallazzini, Morgan [1 ,2 ]
Pallet, Nicolas [1 ,2 ,3 ,4 ,5 ]
机构
[1] INSERM, CNRS, Inst Necker Enfants Malades, UMR 8253,U1151, Paris, France
[2] Ctr Univ St Peres, INSERM, U1147, Paris, France
[3] Univ Paris 05, Paris, France
[4] Hop Europeen Georges Pompidou, Serv Nephrol, Paris, France
[5] Hop Europeen Georges Pompidou, Serv Biochim, Paris, France
关键词
acute kidney injury; chronic kidney disease; endoplasmic reticulum stress; proteinuria; unfolded protein response; UNFOLDED PROTEIN RESPONSE; EPITHELIAL-MESENCHYMAL TRANSITION; ER-STRESS; DIABETIC-NEPHROPATHY; CHEMICAL CHAPERONE; OXIDATIVE STRESS; RENAL FIBROSIS; TUBULAR CELLS; INJURY; DISEASE;
D O I
10.1111/boc.201800019
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:205 / 216
页数:12
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