抗血小板药物治疗反应多样性与对氧磷酶1/血小板内皮聚集受体1基因相关性研究进展

抗血小板聚集药物是脑梗死患者的标准化治疗方案主要药物之一，在二级预防中占重要地位。但是，抗血小板药物疗效有很大个人差异，即抗血小板药物治疗反应多样性（VPR），其可能导致缺血性脑血管病的复发。影响VPR的因素有很多，其中遗传因素发挥重要作用。近年来有两个基因位点研究较多，对氧磷酶1（PON1）基因Q192R位点和血小板内皮聚集受体1（PEAR1）基因rs12041331位点，基因多态性和甲基化共同控制PON1酶和PEAR1受体的浓度或数量水平，从而影响药物代谢。该文拟对以上两个基因位点的基因多态性及其甲基化分别与VPR和缺血性不良事件的相关性进行综述，旨在为抗血小板药物治疗相关研究提供新的依据。

Research advances in the association between variability in response to antiplatelet drugs and paraoxonase-1/platelet endothelial aggregation receptor-1 genes

Antiplatelet drugs have been used in the standardized treatment of cerebral infarction and play an important role in secondary prevention of this disease. However, the interindividual variability in response to antiplatelet drugs (VPR) is likely to cause recurrence of ischemic cerebrovascular disease. The genetic factor is one of many key factors influencing VPR. Two genetic loci, Q192R in the paraoxonase-1 (PON1) gene and rs12041331 in the platelet endothelial aggregation receptor-1 (PEAR1) gene, have been extensively studied in recent years. Gene polymorphisms and methylation co-regulate the concentration or number of PON1 and PEAR1 and finally have an impact on drug metabolism. In order to provide new insights into treatment with antiplatelet drugs, this article reviews the association of gene polymorphisms and methylation at the above two genetic loci with VPR and ischemic events.