Ucp3, short for Uncoupling protein-3, is a mitochondria-regulatory protein belonging to the mitochondrial uncoupling protein family. It is mainly expressed in skeletal muscle, and is thought to play a role in energy metabolism-related pathways, potentially influencing processes like substrate utilization, lipid oxidation, and glucose metabolism. Genetic models, such as gene knockout mouse models, are valuable tools in studying its functions [1,2,3,6].

In Ucp3-knockout (Ucp3-KO) mice, several phenotypes have been observed. In the context of myocardial ischemia-reperfusion (IR) injury, Ucp3-KO mice had larger infarct sizes, higher creatine kinase levels in the effluent, more pronounced mitochondrial structural changes, and exacerbated superoxide production, indicating that Ucp3 deficiency increases the vulnerability of the myocardium to IR injury [7]. In CD4+ T cells, Ucp3-KO cells had increased FoxP3 expression under iTreg conditions and a significantly lower concentration of IL-17A under Th17-inducing conditions, suggesting Ucp3 acts to restrict naive T-cell activation and affects the Th17:Treg cell balance [4]. Additionally, in a rat model of Ucp3 haploinsufficiency (ucp3+/-), it was found that decreased Ucp3 promoted left ventricular diastolic dysfunction during hypertension, as evidenced by worsened diastolic function parameters and decreased exercise tolerance [5].

In conclusion, Ucp3 is involved in multiple biological processes. Through model-based research, especially the use of Ucp3-KO mouse models, its importance in conditions such as myocardial ischemia-reperfusion injury, T-cell differentiation, and left ventricular diastolic dysfunction during hypertension has been revealed. Understanding Ucp3's functions provides insights into the mechanisms of these disease-related processes, potentially offering new directions for disease treatment and prevention.