Mitochondrial Dysfunction as a Pathophysiological Bridge between Metabolic Dysfunction-Associated Fatty Liver Disease and Chronic Kidney Disease
Congwei You1,#, Anwen Yin2,#, Jia Xia3, Le Zhang4,*, Xiaolei Wang1,*, Yutong Hou4,*
1 Department of Pediatrics, The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi People’s Hospital, Wuxi Medical Center, Nanjing Medical University, Wuxi, 214023, China
2 Department of Cardiology, The Affiliated Wuxi People’s Hospital of Nanjing Medical University, Wuxi People’s Hospital, Wuxi Medical Center, Nanjing Medical University, Wuxi, 214023, China
3 Department of Nephrology, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, 200127, China
4 Department of Pediatric Laboratory, Affiliated Children’s Hospital of Jiangnan University, Wuxi Children’s Hospital, Wuxi, 214023, China
* Corresponding Author: Le Zhang. Email: 
; Xiaolei Wang. Email: 
; Yutong Hou. Email: 
# These authors contributed equally to this work as the first author
BIOCELL https://doi.org/10.32604/biocell.2025.072971
Received 08 September 2025; Accepted 14 November 2025; Published online 22 December 2025
Abstract
Metabolic dysfunction-associated fatty liver disease (MAFLD) and chronic kidney disease (CKD) have shown a marked global increase in prevalence, placing a substantial burden on public health and healthcare systems worldwide. Epidemiological data demonstrate a significant overlap between these two conditions, with further evidence from research identifying common pathophysiological features, such as lipid metabolism dysregulation, disrupted energy balance, and chronic systemic inflammation. Mitochondria are central to the pathophysiology of both diseases. In addition to their role in energy production, mitochondria are involved in numerous critical cellular processes, including biosynthesis, lipid metabolism, oxidative phosphorylation, signal transduction, and apoptosis regulation. Mitochondrial dysfunction, characterized by increased reactive oxygen species, impaired adenosine triphosphate synthesis, disrupted mitophagy, and changes in mitochondrial morphology, is implicated in the progression of both MAFLD and CKD. Given the pivotal role of mitochondria in maintaining cellular metabolism homeostasis, dysfunction of this organelle is increasingly recognized as a key mechanistic link that connects the pathophysiological processes underlying both MAFLD and CKD. This review underscores mitochondrial dysfunction as a pathogenic nexus between MAFLD and CKD and examines the mechanisms that drive their pathogenesis
Keywords
Mitochondrial dysfunction; oxidative stress; lipid metabolism; metabolic dysfunction-associated fatty liver disease (MAFLD); chronic kidney disease (CKD); liver-kidney crosstalk
Open Access
Login
Register
Submit a Paper
Propose a Special lssue
Download PDF
Downloads
Citation Tools
