Endoplasmic reticulum stress and kidney dysfunction
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 authorCorresponding 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 authorCorresponding 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 authorCorresponding 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 authorAbstract
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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