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的调控

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细胞损伤释放出大量 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。

ATP, substantially liberated from the injured cells, activates the inflammatory cells to secrete various inflammatory factors, thus triggering cascade inflammation and thrombosis with aggravating the degree of damage. As a " switch” of the inflammatory response and consisting of adenosine (Ado) synthase CD39-CD73, nucleoside transporters (NTs) and termination system of adenosine deaminase (ADA) and adenosine kinase (ADK), the adenosine 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 focus 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; ATP; adenosine; inflammatory

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