过刊浏览

线粒体动力学调控机制及其在肾脏病理生理学中的作用

谭子璇, 朱武政^*

湖南师范大学生命科学学院动物营养与人体健康实验室，长沙 410081

摘要

线粒体是一种动态变化的细胞器，它通过不断的融合、分裂来维持线粒体的形态、数量和功能稳定，这一过程称为线粒体动力学，是线粒体质量控制的重要机制。线粒体的过度融合与分裂都会导致线粒体动力学的稳态失衡，引起线粒体功能障碍，导致细胞损伤甚至死亡。肾脏的生理活动主要由线粒体供能，线粒体动力学稳态失衡影响着线粒体功能，与急性肾损伤、糖尿病肾病等肾脏疾病密切相关。本文对线粒体动力学的调节、线粒体动力学稳态失衡如何导致线粒体损伤以及线粒体损伤对肾脏病理生理学的影响进行综述，以加深对肾脏疾病中线粒体作用的理解与认识。

关键词： 线粒体融合; 线粒体分裂; 肾脏疾病

Regulatory mechanisms of mitochondrial dynamics and its emerging role in renal pathophysiology

TAN Zi-Xuan, ZHU Wu-Zheng^*

Laboratory of Animal Nutrition and Human Health, College of Life Science, Hunan Normal University, Changsha 410081, China

Abstract

Mitochondria are dynamically changing organelles that maintain stable mitochondrial morphology, number, and function through constant fusion and division, a process known as mitochondrial dynamics, which is an important mechanism for mitochondrial quality control. Excessive fusion and division of mitochondria can lead to a homeostatic imbalance in mitochondrial dynamics, causing mitochondrial dysfunction, leading to cellular damage, and even death. The physiological functions of the kidney are mainly powered by mitochondria, and homeostatic imbalance in mitochondrial dynamics affects mitochondrial function and is closely related to renal diseases such as acute kidney injury and diabetic nephropathy. This article reviews the regulation of mitochondrial kinetics, how imbalances in mitochondrial kinetic homeostasis affect mitochondrial injury, and the impact of mitochondrial injury on renal pathophysiology, in order to improve understanding and knowledge of the role of mitochondria in renal disease.

Key words: mitochondrial fusion; mitochondrial fission; renal disease

收稿日期：　　录用日期：

通讯作者：朱武政　　E-mail: zhuwuzheng8@163.com

DOI: 10.13294/j.aps.2024.0011

引用本文：

谭子璇, 朱武政. 线粒体动力学调控机制及其在肾脏病理生理学中的作用[J]. 生理学报 2024; 76 (1): 148-160.

TAN Zi-Xuan, ZHU Wu-Zheng. Regulatory mechanisms of mitochondrial dynamics and its emerging role in renal pathophysiology. Acta Physiol Sin 2024; 76 (1): 148-160 (in Chinese with English abstract).