细胞损伤中腺苷代谢通路与促炎因子调控的研究进展  

Research progress on metabolic pathway of adenosine and regulation of proinflammatory cytokines in cell injury

作　　者：苏晓阳 李少彬[1] 闫玉生[1] SU Xiaoyang;LI Shaobin;YAN Yusheng(Department of Cardiothoracic Surgery,Zhujiang Hospital,Southern Medical University,Guangzhou,510282,P.R.China)

机构地区：[1]南方医科大学珠江医院胸心外科,广州510282

出　　处：《中国胸心血管外科临床杂志》2018年第12期1091-1095,共5页Chinese Journal of Clinical Thoracic and Cardiovascular Surgery

基　　金：2017年度海珠区科技计划项目(海科工商信计2018-97)

摘　　要：细胞损伤释放出大量三磷酸腺苷(adenosine triphophate,ATP),激活炎症细胞产生多种炎症因子,从而引发瀑布式炎症反应及血栓形成,加重损伤程度。腺苷(adenosine,Ado)代谢通路由Ado合成酶CD39-CD73、核苷转运体(nucleoside transporters,NTs)及代谢关键酶—腺苷脱氨酶(adenosine deaminase,ADA)、腺苷激酶(adenosine kinase,ADK)组成,能将促炎因子ATP转化为抗炎介质Ado,如同炎症反应的"开关",调节促炎与抗炎平衡,影响损伤的转归。本文就近年来腺苷代谢通路在细胞损伤中的进展进行综述。Adenosine triphophate(ATP),substantially liberated from the injured cells,activates the inflammatory cells to secrete various inflammatory factors,thus triggering uncontrolled systemic inflammatory response and thrombosis with aggravating the degree of damage.Metabolic pathway of adenosine consists of adenosine(Ado)synthase CD39- CD73,nucleoside transporters(NTs)and termination system of adenosine deaminase(ADA)and adenosine kinase (ADK).As a"switch"of the inflammatory response,the metabolic pathway converts ATP(the pro-inflammatory cytokines)to Ado(the anti-inflammatory mediators),maintaining the homeostasis between pro-inflammatory and anti- inflammatory as well as affecting the outcome of the injury.This review focused on the recent progress of adenosine metabolic pathway in cell injury.

关 键 词：缺血再灌注损伤 三磷酸腺苷 腺苷 炎症 

分 类 号：R363[医药卫生—病理学]