The role of mitophagy in the development of chronic kidney disease

Abstract

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.

Insights into the role of mitophagy in lung cancer: current evidence and perspectives

“…Mitophagy, a critical cellular process, involves the selective degradation of mitochondria through autophagy, and plays a crucial role in maintaining mitochondrial quality control and cellular homeostasis ( Pickles et al, 2018 ; Filippelli et al, 2022 ; Yang et al, 2024 ).…”

“…The primary modalities that govern mitophagy encompass ubiquitin-dependent, receptor dependent, and other pathways ( Ma et al, 2023 ; Tang et al, 2024 ). The process begins with the recognition and tagging of damaged or dysfunctional mitochondria by specific proteins, such as Parkin, proteins like PTEN-induced kinase 1 (PINK1), Bcl-2/adenovirus E1B 19-kDa-interacting protein 3 (BNIP3), and Nix ( Wu et al, 2023 ; Yang et al, 2024 ). These proteins work together to target the damaged mitochondria for degradation.…”