阿司匹林抵抗相关的基因多态性与血小板反应性的研究进展

Advances in the study on aspirin resistance-related gene polymorphisms and platelet reactivity

阿司匹林是目前使用最多的抗血小板药物,但相同的剂量在不同个体中会有血小板反应性的差异,其中最常见的原因是阿司匹林低反应或无反应的患者服用阿司匹林后不能引起血小板功能测定的预期改变,心脑血管事件复发,出现阿司匹林抵抗(AR)现象。据统计,高达30%的血小板活性变异可以由遗传因素解释,目前新的研究提出基因交互作用对AR的贡献更有意义。本综述将从环氧合酶(COX)-1、COX-2、血红素加氧酶-1、血小板受体(二磷酸腺苷受体、纤维蛋白原受体、胶原受体)、血小板内皮素受体-1、前列腺素内过氧化物合酶1、基因-基因交互作用等方面评估AR相关的基因多态性对血小板反应性的影响。

Aspirin is currently the most used antiplatelet drug,but the same dose of aspirin may cause platelet reactivity differences in different individuals,the most common reason for which is the failure of patients with low or no response to aspirin to induce the expected changes in platelet function measurements,recurrence of cardiovascular events,and the occurrence of aspirin resistance(AR).Statistically,genetic factors can explain up to 30%of the variation in platelet activity,and new studies suggest that gene-gene interactions are of more significant contribution to AR.This paper of review will assess the impact of AR-related gene polymorphisms on platelet reactivity in terms of cyclooxygenases(COX)-1,COX-2,heme oxygenase-1,platelet receptors(adenosine diphosphate receptor,fibrinogen receptor,collagen receptor),platelet endothelin receptor-1,prostaglandin endoperoxide synthase 1,and gene-gene interactio ns.