蛋白激酶Cη基因与腔隙性脑梗死

摘要

蛋白激酶C(protein kinase C,PKC)是细胞内信号转导的重要信使.迄今为止,已分离纯化至少11种PKC亚型.PKCη亚型基因PRKCH的非同义单核苷酸突变(1425G/A)可导致PKCη活性增高,被认为是腔隙性脑梗死的一个新型危险因素.近年来,有关PRKCH在细胞分化和凋亡中的作用以及与一些信号转导通路关系等方面的研究有了一些新的进展,特别是PKCη参与了丝裂原活化蛋白激酶、诱导型一氧化氮合酶、基质金属蛋白酶等与动脉粥样硬化过程密切相关的一些关键酶活性的调节,为今后脑梗死的临床干预提供了新的思路.%Protein Kinase C (PKC) is an important messenger in intracellular signal transduction. So far, at least 11 members of PKC isoforms have been isolated and purified. The mutation of the non-synonymous SNP (1425G/A) of the η isoform of protein kinase C (PKC η), a protein kinase Cη gene (PRKCH) may result in the increased PKCη activity, which is considered as a new risk factor for lacunar infarction. In recent years, the studies about the role of PRKCH in cell differentiation and apoptosis and its relation with some signal transduction pathways have made some new advances, especially, PKCη participates in the regulation of some key enzyme activity that mitogen-activated protein kinase, inducible nitric oxide-synthase and matrix metalloproteinase are closely correlated with the process of atherosclerosis. It will provide a new way of thinking for the clinical intervention of cerebral infarction in the future.