关键词: 糖尿病肾脏疾病, 线粒体 DNA, 生物标志物

Abstract: Mitochondrial dysfunction is one of the central pathologic links in diabetic kidney disease (DKD). As the crucial genetic material of mitochondria, mitochondrial DNA (mtDNA) damage plays a significant role in the progression of DKD. This review systematically elaborates on the mechanisms by which hyperglycemia, oxidative stress, lipotoxicity, and mitochondrial dynamics abnormalities induce mtDNA damage under DKD conditions. Focusing on renal intrinsic cells, it highlights the molecular mechanisms through which mtDNA damage drives DKD progression, including disruptions in energy metabolism, exacerbation of oxidative stress, induction of apoptosis, activation of inflammatory responses, and interference with mitophagy. Furthermore, this article summarizes current therapeutic strategies targeting mtDNA, and discusses the potential and challenges of using mtDNA copy number in peripheral blood or urine as a non⁃invasive biomarker for DKD, aiming to provide new insights and a theoretical basis for the prevention and treatment of DKD.