Volume 110, Issue 9 pp. 205-216
Review

Endoplasmic reticulum stress and kidney dysfunction

Morgan Gallazzini

Corresponding Author

Morgan Gallazzini

INSERM U1151 - CNRS UMR 8253, Institut Necker Enfants Malades, Paris, France

INSERM U1147, Centre Universitaire des Saints Pères, Paris, France

To whom correspondence should be addressed (Email [email protected] and [email protected])Search for more papers by this author
Nicolas Pallet

Corresponding Author

Nicolas Pallet

INSERM U1151 - CNRS UMR 8253, Institut Necker Enfants Malades, Paris, France

INSERM U1147, Centre Universitaire des Saints Pères, Paris, France

Université Paris Descartes, Paris, France

Service de Néphrologie, Hôpital Européen Georges Pompidou, Paris

Service de Biochimie, Hôpital Européen Gorges Pompidou, Paris, France

To whom correspondence should be addressed (Email [email protected] and [email protected])Search for more papers by this author
First published: 10 July 2018
Citations: 52

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.

Conflict of interest statement

The authors have declared no conflict of interest.

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