Department of Emergency Medicine, Tianjin Medical University General Hospital, Tianjin, China.
Ren Fail. 2024 Dec;46(2):2393262. doi: 10.1080/0886022X.2024.2393262. Epub 2024 Aug 27.
Acute kidney injury (AKI) is a systemic clinical syndrome increasing morbidity and mortality worldwide in recent years. Renal tubular epithelial cells (TECs) death caused by mitochondrial dysfunction is one of the pathogeneses. The imbalance of mitochondrial quality control is the main cause of mitochondrial dysfunction. Mitochondrial quality control plays a crucial role in AKI. Mitochondrial quality control mechanisms are involved in regulating mitochondrial integrity and function, including antioxidant defense, mitochondrial quality control, mitochondrial DNA (mtDNA) repair, mitochondrial dynamics, mitophagy, and mitochondrial biogenesis. Currently, many studies have used mitochondrial dysfunction as a targeted therapeutic strategy for AKI. Therefore, this review aims to present the latest research advancements on mitochondrial dysfunction in AKI, providing a valuable reference and theoretical foundation for clinical prevention and treatment of this condition, ultimately enhancing patient prognosis.
急性肾损伤（AKI）是近年来全球范围内发病率和死亡率增加的一种系统性临床综合征。由线粒体功能障碍引起的肾小管上皮细胞（TEC）死亡是其发病机制之一。线粒体质量控制失衡是线粒体功能障碍的主要原因。线粒体质量控制在 AKI 中起着至关重要的作用。线粒体质量控制机制参与调节线粒体的完整性和功能，包括抗氧化防御、线粒体质量控制、线粒体 DNA（mtDNA）修复、线粒体动力学、线粒体自噬和线粒体生物发生。目前，许多研究已将线粒体功能障碍作为 AKI 的靶向治疗策略。因此，本综述旨在介绍 AKI 中线粒体功能障碍的最新研究进展，为临床预防和治疗该病提供有价值的参考和理论基础，最终改善患者预后。
