Mitochondrial Dysfunction as a Pathophysiological Bridge between Metabolic Dysfunction-Associated Fatty Liver Disease and Chronic Kidney Disease

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