Related Experiment Video
Updated: Feb 8, 2026

Visualization of Endoplasmic Reticulum Subdomains in Cultured Cells
Published on: February 18, 2014
Endoplasmic reticulum stress and kidney dysfunction
Morgan Gallazzini1,2, Nicolas Pallet1,2,3,4,5
1INSERM U1151 - CNRS UMR 8253, Institut Necker Enfants Malades, Paris, France.
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.
Insights
Endoplasmic reticulum (ER) stress is implicated in kidney injury, contributing to both damage and adaptation in acute kidney injury (AKI) and chronic kidney disease (CKD). This review analyzes ER stress
Area of Science:
- Nephrology
- Molecular Biology
- Cellular Biology
Background:
- Chronic kidney disease (CKD) is a global health issue requiring better therapeutic strategies.
- Acute kidney injury (AKI) significantly contributes to chronic histological damage in CKD.
- Cellular responses to kidney injury involve microenvironmental changes and adaptive processes.
Purpose of the Study:
- To review the role of endoplasmic reticulum (ER) stress in AKI and CKD pathophysiology.
- To critically analyze evidence linking ER stress to kidney damage.
- To explore ER stress's dual role in kidney injury and protection.
Main Methods:
- Literature review of experimental and clinical studies.
- Analysis of molecular and cellular mechanisms.
- Synthesis of current evidence on ER stress in kidney disease.
Main Results:
- ER stress is a common cellular response to kidney injury.
- ER stress contributes to both acute and chronic kidney damage.
- ER stress also plays a role in cellular adaptation and nephroprotection.
Conclusions:
- ER stress is a key mediator in the pathophysiology of AKI and CKD.
- Understanding ER stress mechanisms is crucial for developing novel therapeutic interventions.
- Further research is needed to fully elucidate ER stress's complex role in kidney health and disease.
Related Concept Videos
Endoplasmic Reticulum
The Endoplasmic Reticulum
Smooth Endoplasmic Reticulum
The ER provides optimal conditions for synthesizing steroid hormones and lipids, such as phospholipids and triglycerides. Traditionally, lipid metabolism was considered to be a smooth ER function. However, there is no direct evidence to prove that rough ER is completely excluded from lipid...
Directing Proteins to the Rough Endoplasmic Reticulum
Kidney Structure
Responses to Salt Stress

