新近研究发现阻断高血糖引起的线粒体活性氧簇(ROS)的产生可以阻断所有高血糖引起的损伤。而线粒体ROS产生与线粒体内膜上的脱偶联蛋白(UCP)密切相关。ROS可以引起UCP表达增加,UCP超表达或脱偶联剂可以阻断高血糖引起的ROS的产生,UCP-2超表达可以抑制线粒体ROS的产生,提示脱偶联蛋白可能与糖尿病微血管并发症的发生密切相关。 Recent studies have found that blocking hyperglycemia-induced production of mitochondrial reactive oxygen species (ROS) can block all hyperglycemic-induced damage. Mitochondrial ROS production is closely related to the uncoupling protein (UCP) in the mitochondrial inner membrane. ROS can cause increased UCP expression, UCP over-expression or uncoupling agent can block the production of high blood sugar ROS, UCP-2 overexpression can inhibit the production of mitochondrial ROS, suggesting that the uncoupling protein may be associated with diabetic microvascular complications Closely related.