Diabetic kidney disease (DKD) is a significant complication of diabetes and a major cause of end-stage renal disease. Affecting around 40% of diabetic patients, DKD poses substantial economic burdens due to its prevalence worldwide. The primary clinical features of DKD include the leakage of proteins into the urine, altered glomerular filtration, and an increased risk of cardiovascular diseases. Current treatments focus on managing hypertension and hyperglycemia to slow the progression of DKD. These include the use of SGLT2 inhibitors to control blood sugar and ACE inhibitors to reduce blood pressure. Despite these measures, current treatments do not cure DKD and fail to address its underlying causes. Emerging research highlights mitochondrial dysfunction as a pivotal factor in DKD progression. The kidneys' high energy requirements make them particularly susceptible to disturbances in mitochondrial function. In DKD, mitochondrial damage leads to reduced energy production and increased oxidative stress, exacerbating tissue damage. Mitochondrial DNA (mtDNA) damage is a key aspect of this dysfunction, with studies suggesting that changes in mtDNA copy number can serve as biomarkers for the progression of the disease. Efforts to target mitochondrial dysfunction are gaining traction as a potential therapeutic strategy. This includes promoting mitochondrial health through pharmacological and lifestyle interventions aimed at enhancing mitochondrial function and reducing oxidative stress. Such approaches could lead to more effective treatments that directly address the DKD.
Keywords: TFAM; diabetic kidney disease; mitochondrial DNA; mitochondrial dysfunction; oxidative stress.
© 2024 Yu et al.