摘要
SLE的表观遗传学研究显示，DNA低甲基化状态在SLE发病机制中具有重要作用。DNA甲基转移酶是DNA甲基化反应的催化剂，是干预DNA甲基化状态的重要物质。DNA甲基转移酶的转录水平和活性受启动子表位修饰、信号传导与转录激活因子3、肿瘤抑制基因p53、转录因子家族sp蛋白、甲基化CG序列结合蛋白等多种因素调控。狼疮患者DNA甲基转移酶的表达与活性降低，并与T淋巴细胞DNA低甲基化发生机制相关。探讨DNA甲基转移酶在SLE表观遗传学发病机制中的作用通路，揭示SLE表观遗传学的调控机制，将为SLE治疗提出新的治疗方案。
Epigenetic studies have indicated the importance of DNA hypomethylation in the etiology of systemic lupus erythematosus （SLE）. DNA methyltransferases is the catalyst of DNA methylation reaction, as well as an important molecule interfering the methylation level. The mRNA transcriptional level and activity of DNA methyltransferases are regulated by various factors, such as promoter epitope modification, signal transducer and activator of transcription-3 （STAT3）, transcription factor Spl and Sp3, tumor-suppressing gene p53, methyl-CpG binding proteins （MeCP2）, and so on. The expression and activity of DNA methyltransferases are dowitregulated in patients with lupus erythematous, which is linked with the DNA hypomethylation of T cells. To investigate the action pathway of DNA methyltransferases in the epigenetic pathogenesis of systemic lupus erythematosus, and to disclose the regulation mechanism of epigenetic inheritance of systemic lupus erythematosus, may provide new strategies and regimens for the treatment of this disease.
出处
《国际皮肤性病学杂志》
2009年第2期90-92,共3页
International Journal of Dermatology and Venereology
基金
上海市科委资助课题（064119529）
