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.

中文翻译：

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内质网应激与肾功能障碍

慢性肾病 (CKD) 影响着全世界数百万人，并构成了一个重大的公共卫生问题。因此，了解 CKD 的分子基础是制定预防和治疗策略的关键挑战。与 CKD 相关的慢性组织学损伤的一个主要因素是急性肾损伤 (AKI)。在细胞水平上，肾脏损伤与微环境改变有关，迫使细胞激活适应性生物过程，以消除压力源并产生警报信号。这些信号通路通过促进炎症和纤维生成积极参与组织重塑，最终导致 CKD。肾损伤时遇到的许多压力都容易引发内质网 (ER) 压力。在肾脏中，内质网应激既参与急性和慢性组织学损伤，也促进细胞适应和肾脏保护。在这篇综述中，我们将讨论 ER 应激在 AKI 和 CKD 进展的病理生理学中的意义，我们将对当前支持 ER 应激作为肾损伤介质的实验和临床证据进行批判性分析。