解偶联蛋白2在内皮损伤及血管重构中的作用研究进展

心脑血管疾病是全球最主要的致死性疾病。活性氧(Reactive oxygen species,ROS)产生增多诱发血管内皮细胞损伤、平滑肌细胞迁移、增殖,是导致血管功能障碍、血管重构发生的重要机制。因此,氧化应激被认为是心脑血管疾病发生、发展的关键环节。但通过补充外源性抗氧化剂防治心脑血管疾病一直存在较大争议。机体可通过自身防御体系拮抗氧化应激,维持氧化-还原状态,如通过调控线粒体解偶联蛋白2(Uncoupling protein 2,UCP2)调节ROS生成,改善血管功能障碍及血管重构。本文就UCP2在内皮损伤及血管重构中的作用及机制展开综述,为深入探索这一潜在的防治心脑血管疾病的靶点提供信息。

Research Progress on the Role of Uncoupling Protein 2 in Endothelial Injury and Arterial Remodeling

ABSTRACT: Cardiovascular and cerebrovascular diseases are the leading causes of death on the world. Excessive reactive oxygen species(ROS), inducing the injury of vascular endothelial cells and migration and proliferation of smooth muscle cells, is an important mechanism for the occurrence of vascular dysfunction and arterial remodeling. Therefore, oxidative stress is considered as a key link in the occurrence and development of cardiovascular and cerebrovascular diseases. However, there is still remaining controversial for the treatment of cardiovascular and cerebrovascular diseases by supplementing exogenous antioxidants. The body can antagonize oxidative stress through its own defense system, maintain the oxidation-reduction state, and initiate endogenous protective mechanisms against the production of superoxide anions. For instance, by regulating mitochondrial uncoupling protein 2(UCP2), ROS production can be regulated, improving vascular dysfunction and arterial remodeling. In this review, the roles and mechanisms of UCP2 in endothelial injury and arterial remodeling were summarized, in order to provide information for further exploration of this potential target for prevention and treatment of cardiovascular and cerebrovascular diseases.