Department of Pathophysiology, School of Basic Medical Sciences, Shandong Second Medical University, Weifang, Shandong, China.
School of Clinical Medicine, Shandong Second Medical University, Weifang, Shandong, China.
PeerJ. 2024 Apr 25;12:e17260. doi: 10.7717/peerj.17260. eCollection 2024.
Chronic kidney disease (CKD) represents a significant global health concern, with renal fibrosis emerging as a prevalent and ultimate manifestation of this condition. The absence of targeted therapies presents an ongoing and substantial challenge. Accumulating evidence suggests that the integrity and functionality of mitochondria within renal tubular epithelial cells (RTECs) often become compromised during CKD development, playing a pivotal role in the progression of renal fibrosis. Mitophagy, a specific form of autophagy, assumes responsibility for eliminating damaged mitochondria to uphold mitochondrial equilibrium. Dysregulated mitophagy not only correlates with disrupted mitochondrial dynamics but also contributes to the advancement of renal fibrosis in CKD. While numerous studies have examined mitochondrial metabolism, ROS (reactive oxygen species) production, inflammation, and apoptosis in kidney diseases, the precise pathogenic mechanisms underlying mitophagy in CKD remain elusive. The exact mechanisms through which modulating mitophagy mitigates renal fibrosis, as well as its influence on CKD progression and prognosis, have not undergone systematic investigation. The role of mitophagy in AKI has been relatively clear, but the role of mitophagy in CKD is still rare. This article presents a comprehensive review of the current state of research on regulating mitophagy as a potential treatment for CKD. The objective is to provide fresh perspectives, viable strategies, and practical insights into CKD therapy, thereby contributing to the enhancement of human living conditions and patient well-being.
慢性肾脏病（CKD）是一个全球性的健康问题，肾纤维化是 CKD 的一种普遍且最终的表现形式。目前缺乏靶向治疗方法，这是一个持续存在的重大挑战。越来越多的证据表明，在 CKD 发展过程中，肾脏管状上皮细胞（RTEC）内的线粒体完整性和功能通常会受到损害，在肾纤维化的进展中起着关键作用。自噬是一种特殊形式的自噬，负责清除受损的线粒体以维持线粒体平衡。自噬失调不仅与线粒体动力学的破坏有关，而且还促进 CKD 中的肾纤维化进展。虽然许多研究已经研究了线粒体代谢、ROS（活性氧）产生、炎症和细胞凋亡在肾脏疾病中的作用，但 CKD 中自噬的具体发病机制仍不清楚。调节自噬减轻肾纤维化的具体机制，以及其对 CKD 进展和预后的影响，尚未经过系统研究。自噬在 AKI 中的作用相对明确，但自噬在 CKD 中的作用仍很少见。本文对调节自噬作为 CKD 潜在治疗方法的研究现状进行了全面综述。目的是为 CKD 治疗提供新的视角、可行的策略和实用的见解，从而改善人类的生活条件和患者的健康状况。
