Li Zixian, Liu Zejian, Luo Mianna, Li Xingyu, Chen Huixia, Gong Siqiao, Zhang Minjie, Zhang Yaozhi, Liu Huafeng, Li Xiaoyu
Institute of Nephrology, and Guangdong Provincial Key Laboratory of Autophagy and Major Chronic Non-communicable Diseases, Affiliated Hospital of Guangdong Medical University, Zhanjiang, 524001, China.
Cell Death Discov. 2022 May 2;8(1):239. doi: 10.1038/s41420-022-01034-0.
Acute kidney injury (AKI) is a common clinical condition associated with high morbidity and mortality. The pathogenesis of AKI has not been fully elucidated, with a lack of effective treatment. Renal tubular epithelial cells (TECs) play an important role in AKI, and their damage and repair largely determine the progression and prognosis of AKI. In recent decades, it has been found that the mitochondria, endoplasmic reticulum (ER), lysosomes, and other organelles in TECs are damaged to varying degrees in AKI, and that they can influence each other through various signaling mechanisms that affect the recovery of TECs. However, the association between these multifaceted signaling platforms, particularly between mitochondria and lysosomes during AKI remains unclear. This review summarizes the specific pathophysiological mechanisms of the main TECs organelles in the context of AKI, particularly the potential interactions among them, in order to provide insights into possible novel treatment strategies.
急性肾损伤（AKI）是一种常见的临床病症，具有高发病率和死亡率。AKI的发病机制尚未完全阐明，且缺乏有效的治疗方法。肾小管上皮细胞（TECs）在AKI中起重要作用，其损伤和修复在很大程度上决定了AKI的进展和预后。近几十年来，人们发现TECs中的线粒体、内质网（ER）、溶酶体等细胞器在AKI中会受到不同程度的损伤，并且它们可以通过各种信号机制相互影响，进而影响TECs的恢复。然而，在AKI期间，这些多方面信号平台之间的关联，尤其是线粒体和溶酶体之间的关联仍不清楚。本综述总结了在AKI背景下主要TECs细胞器的具体病理生理机制，特别是它们之间的潜在相互作用，以便为可能的新型治疗策略提供见解。
