Role of protease-activated receptor 2 in metabolic syndrome

代谢综合征（MetS）的特征是动脉粥样硬化风险的累积。增加内脏肥胖是由于心血管并发症的发展综合征通过过度生产的炎症因子释放的脂肪细胞。然而，蛋白酶激活受体2（PAR2）在MetS血管反应性中的作用尚未完全了解。因此，我们研究了PAR2介导的血管舒张的变化，使用动物模型的MetS.Our研究表明，PAR2介导的血管舒张被保存，即使一氧化氮（NO）介导的血管舒张由其他激动剂受损的动脉MetS大鼠。内皮NO合酶的增强可能在PAR 2介导的血管舒张功能的维持中起重要作用。此外，我们建议，血管周围的脂肪组织包裹在血管增强NO介导的血管舒张的病理生理条件下，以弥补受损的血管舒张代谢综合征。

Metabolic syndrome (MetS) is characterized by accumulation of atherosclerotic risk. Increased visceral adiposity is attributed to the development of cardiovascular complications in the syndrome via overproduction of inflammatory factors released from adipocytes. However, the role of protease-activated receptor 2 (PAR2) in vascular responsiveness in MetS is not fully understood. Therefore, we studied changes in PAR2-mediated vasodilation using an animal model of MetS.Our study demonstrates that PAR2-mediated vasodilation is preserved even though nitric oxide (NO)-mediated vasodilation by other agonists is impaired in arteries of MetS rats. Enhancement of endothelial NO synthase may play important role in the preservation of PAR2-mediated vasodilation. Furthermore, we propose that perivascular adipose tissue wrapped around the blood vessel enhances NO-mediated vasodilation under pathophysiological conditions to compensate for impaired vasodilation in MetS.