线粒体功能障碍相关足细胞损伤在糖尿病肾脏疾病中的研究进展OA

Diabetic kidney disease(DKD)is a leading cause of end-stage renal disease,characterized by pathological changes including decreased glomerular filtration rate and proteinuria.As a key component of the glomerular filtration barrier,podocyte injury is closely associated with the progression of DKD.Recent studies revealed that mitochondrial dysfunction plays a central role in podocyte injury in DKD,primarily manifested as enhanced mitochondrial oxidative stress,defective autophagy,and fission/fusion imbalance.These alterations lead to the excessive production of reactive oxygen species and inflammatory factors,thereby accelerating podocyte apoptosis.Multiple signaling pathways,including NADPH oxidase 4/transient receptor potential cation channel subfamily C member 6,transforming growth factor β1/SMAD,AMP-activated protein kinase/peroxisome proliferator-activated receptor gamma coactivator 1α,and PTEN induced kinase 1/Parkin,can intervene in mitochondrial damage-induced podocyte apoptosis,while DKD is exacerbated by the dysregulation of genes related to podocyte mitochondrial function.This review systematically considers the critical roles of relevant signaling pathways and mitochondrial damage in mediating podocyte mitochondrial injury during DKD progression,aiming to provide new theoretical foundations and therapeutic targets for DKD prevention and treatment.We also explore the potential of traditional Chinese medicine targeting podocyte mitochondria as a strategy to delay DKD progression.