Wu Yi-Jin, Yang Yan-Rong, Yan Ya-Ling, Yang Han-Yinan, Du Jun-Rong
Department of Pharmacology, Key Laboratory of Drug-Targeting and Drug Delivery System of the Education Ministry and Sichuan Province, Sichuan Engineering Laboratory for Plant-Sourced Drug and Sichuan Research Center for Drug Precision Industrial Technology, West China School of Pharmacy, Sichuan University, Chengdu, Sichuan, China.
Mol Cell Biochem. 2025 Apr 29. doi: 10.1007/s11010-025-05297-w.
The incidence and hospitalization rate of kidney disease, especially end-stage renal disease, have increased significantly, which seriously endangers the health of patients. Mitochondria are the core organelles of cellular energy metabolism, and their dysfunction can lead to kidney energy supply insufficiency and oxidative stress damage, which has become a global public health problem. Studies have shown that the disturbance of mitochondrial quality control mechanisms, including mitochondrial dynamics, autophagy, oxidative stress regulation and biosynthesis, is closely related to the occurrence and development of renal fibrosis (RF). As a multicellular pathological process, RF involves the injury and shedding of podocytes, the transdifferentiation of renal tubular epithelial cells, the activation of fibroblasts, and the infiltration of macrophages, among which the mitochondrial dysfunction plays an important role. This review systematically elaborates the molecular mechanisms of mitochondrial damage during RF progression, aiming to provide theoretical foundations for developing novel therapeutic strategies to delay RF advancement.
肾脏疾病，尤其是终末期肾病的发病率和住院率显著上升，严重危及患者健康。线粒体是细胞能量代谢的核心细胞器，其功能障碍可导致肾脏能量供应不足和氧化应激损伤，这已成为一个全球性的公共卫生问题。研究表明，线粒体质量控制机制的紊乱，包括线粒体动力学、自噬、氧化应激调节和生物合成，与肾纤维化（RF）的发生发展密切相关。作为一种多细胞病理过程，RF涉及足细胞的损伤和脱落、肾小管上皮细胞的转分化、成纤维细胞的激活以及巨噬细胞的浸润，其中线粒体功能障碍起重要作用。本综述系统阐述了RF进展过程中线粒体损伤的分子机制，旨在为开发延缓RF进展的新型治疗策略提供理论基础。
