JAK2/STAT3介导的内皮细胞黏附在TAO发病机制中的作用  

The Role of JAK2/STAT3 Mediated Endothelial Cell Adhesion in the TAO Pathogenesis

作　　者：邵长刚[1] 刘冰[1] 魏争[1] 

机构地区：[1]哈尔滨医科大学附属第一医院血管外科

出　　处：《医学综述》2016年第2期245-248,共4页Medical Recapitulate

摘　　要：血栓闭塞性脉管炎(TAO)是一类非动脉硬化局限性血管性疾病,致残率较高,多发病于青年,吸烟为主要致病因素,是难治性疾病之一。目前,TAO的治疗以手术为主,其中以腰交感神经节切除合并腘动脉序贯法内膜剥脱法治疗效果较为理想,大量术中标本及病理学支持发现,TAO病变不同于其他血栓性动脉疾病,其血栓成分不仅为血细胞,还含有炎性细胞及免疫细胞。在对TAO的研究中发现,TAO患者高表达细胞炎性因子,这些炎性因子能作用于血管内皮细胞的转导开关Janus激酶2/信号转导转录激活因子3,后者介导血管内皮细胞的黏附作用,参与血管损伤以及血栓形成。Thromboartgiitis ohliterans（TAO） is a class of non-athetnsclerotic limited vascular disease, with high morbidity, usually occurring in young people, and smoking is the major pathogenic factor. It is one of the intractable diseases. Currently, the main treatment of TAO is surgery, among which lumbar sympathec- tomy and popliteal artery sequential endarterectomy is an ideal treatment. A lot of intraoperative pathologic specimens found that TAO lesions are unlike other thrombotic arterial disease, which not only consist blood cells, but also inflammatory cells and immune cells. Studies of TAO found that TAO patients had high expres- sion of cell inflammatory cytokines, which could act on endothelial cells transduced switch JAK2/STAT3, and the latter mediates adhesion of endothelial cells and is involved in vascular injury and thrombosis.

关 键 词：血栓闭塞性脉管炎 内皮黏附 发病机制 

分 类 号：R654.4[医药卫生—外科学]