TET2突变相关不确定潜能的克隆性造血与卒中发生发展的研究进展

Progress of the Relationship between TET2 Mutation Related Clonal Hematopoiesis of Indeterminate Potential and Stroke

与年龄相关的不确定潜能的克隆性造血(clonal hematopoiesis of indeterminate potential,CHIP)能通过激活炎症促进动脉粥样硬化的发生、发展,从而增加心脑血管疾病风险。作为最常见的CHIP相关突变的表观遗传调控基因之一,甲基胞嘧啶双加氧酶2(ten-eleven translocation-2,TET2)基因突变可通过组蛋白去乙酰化作用增加巨噬细胞中IL-1β等促炎因子的转录,加速动脉粥样硬化斑块的形成,并与卒中风险增加及预后不良有关。未来通过靶向TET2基因及其相关机制通路可能有助于发现降低卒中风险或改善卒中预后的新途径。

Age-related clonal hematopoiesis of indeterminate potential(CHIP)promotes the development of atherosclerosis by activating inflammation,which increases the risk of cardiovascular diseases.As one of the most common epigenetic regulatory genes among CHIP,the mutations in the ten-eleven translocation-2(TET2)gene can increase the transcription of inflammatory factors such as IL-1βin macrophages through histone deacetylation.Therefore,it accelerates the development of atherosclerotic plaque,and is related with increasing risk of stroke and poor prognosis.In the future,research on targeting TET2 and its related mechanism pathways may help explore new strategies to reduce the occurrence of stroke and improve the patients’prognosis.