UCP2 is a mitochondrial inner membrane antiporter that exports dicarboxylate intermediates (oxaloacetate, malate, aspartate) from the mitochondrial matrix in exchange for phosphate and protons 1. This transport process reduces ATP/ADP ratios and suppresses reactive oxygen species (ROS) production by limiting acetyl-CoA oxidation through the Krebs cycle 1. UCP2 mediates inducible proton entry and regulates fatty acid metabolism, processes controlled by free fatty acids and purine nucleotides 234. Beyond metabolism, UCP2 regulates glucose-induced mitochondrial fission and modulates ROS levels during macrophage-mediated inflammation resolution 5. Clinically, UCP2 functions as a mechanosensitive suppressor of atherosclerosis; endothelial UCP2 expression is upregulated by unidirectional shear stress via KLF2, and UCP2 deficiency promotes atherosclerosis through FoxO1-mediated inflammation 6. In diabetic retinopathy, hyperglycemia downregulates UCP2, and UCP2 overexpression protects retinal endothelial cells by activating the NAD+-SIRT3 axis to reduce oxidative stress and senescence 7. UCP2 genetic variants associate with disease susceptibility: the -866G/A G/G genotype increases schizophrenia risk 4.377-fold 8, while rs659366 polymorphisms interact with dietary factors to influence congenital heart disease risk 9. These findings establish UCP2 as a central regulator of mitochondrial bioenergetics and oxidative stress with implications for metabolic and vascular diseases.