中国胸心血管外科临床杂志

中国胸心血管外科临床杂志

细胞损伤中腺苷代谢通路与促炎因子调控的研究进展

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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

Key words: Ischemia-reperfusion injury; adenosine triphophate; adenosine; inflammation

引用本文: 苏晓阳, 李少彬, 闫玉生. 细胞损伤中腺苷代谢通路与促炎因子调控的研究进展. 中国胸心血管外科临床杂志, 2018, 25(12): 1091-1095. doi: 10.7507/1007-4848.201803002 复制

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