Mitochondrial dysfunction: the hidden catalyst in chronic kidney disease progression.

Chronic kidney disease (CKD) represents a global health epidemic, with approximately one-third of affected individuals ultimately necessitating renal replacement therapy or transplantation. The kidney, characterized by its exceptionally high energy demands, exhibits significant sensitivity to alterations in energy supply and mitochondrial function. In CKD, a compromised capacity for mitochondrial ATP synthesis has been documented. As research advances, the multifaceted roles of mitochondria, extending beyond their traditional functions in oxygen sensing and energy production, are increasingly acknowledged. Empirical studies have demonstrated a strong association between mitochondrial dysfunction and the pathogenesis of fibrosis and cellular apoptosis in CKD. Targeting mitochondrial dysfunction holds substantial therapeutic promise, with emerging insights into its epigenetic regulation in CKD, particularly involving non-coding RNAs and DNA methylation. This article presents a comprehensive review of contemporary research on mitochondrial dysfunction in relation to the onset and progression of CKD. It elucidates the associated molecular mechanisms across various renal cell types and proposes novel research avenues for CKD treatment.