TET2：动脉粥样硬化的新型表观遗传调控因子和潜在干预靶点。
TET2: A Novel Epigenetic Regulator and Potential Intervention Target for Atherosclerosis.
机构信息
1 Key Laboratory for Atherosclerology of Hunan Province, Institute of Cardiovascular Disease, University of South China , Hengyang, China .
2 Department of Spine Surgery, The First Affiliated Hospital, University of South China , Hengyang, China .
出版信息
DNA Cell Biol. 2018 Jun;37(6):517-523. doi: 10.1089/dna.2017.4118. Epub 2018 Apr 13.
Atherosclerosis is the underlying cause of cardio-cerebrovascular disease. However, the mechanisms of atherosclerosis are still unclear. The modification of DNA methylation has an important role in atherosclerosis development. As a member of the Ten-eleven translocation (TET) family, TET methylcytosine dioxygenase 2 (TET2) can modify DNA methylation by catalyzing 5-methylcytosine to 5-hydroxymethylcytosine and mediate DNA demethylation. Recent findings suggest that TET2 is related to the phenotype transformation of vascular smooth muscle cells, endothelial dysfunction, and inflammation of macrophage, the key factors of atherosclerosis. Therefore, TET2 may be a potential target for atherosclerosis treatment. This review will elaborate the recent findings that suggest the role of TET2 in atherosclerosis.
动脉粥样硬化是心脑血管疾病的根本原因。然而，动脉粥样硬化的机制仍不清楚。DNA 甲基化的修饰在动脉粥样硬化的发展中起着重要作用。作为 Ten-eleven translocation (TET) 家族的一员，TET 甲基胞嘧啶双加氧酶 2 (TET2) 可以通过催化 5-甲基胞嘧啶转化为 5-羟甲基胞嘧啶来修饰 DNA 甲基化，并介导 DNA 去甲基化。最近的研究发现，TET2 与血管平滑肌细胞表型转化、内皮功能障碍和巨噬细胞炎症有关，这些都是动脉粥样硬化的关键因素。因此，TET2 可能是动脉粥样硬化治疗的一个潜在靶点。本综述将详细阐述 TET2 在动脉粥样硬化中的作用的最新发现。
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