摘要越来越多的证据表明,表观遗传学与瘢痕疙瘩形成机制可能相关.与正常皮肤相比,瘢痕疙瘩全基因组胞嘧啶?磷酸二酯键鸟苷岛中低甲基化比高甲基化更常见,且相关基因的启动子区亦存在同样现象.启动子的高甲基化通常发生在易感基因的相同位点,甲基化可能起到早期标记物的作用.去乙酰化酶的表达明显增高,活性增强,基因的组蛋白乙酰化修饰水平降低,细胞凋亡下降,最终促进了瘢痕疙瘩的发生发展.miR?21等23种miRNA表达上调,miR?203等9种miRNA表达下调.表观遗传学路径在瘢痕疙瘩的形成和发展中的作用值得进一步研究.

abstractsMore and more evidences have indicated that epigenetics may be associated with the formation of keloids. Compared with the normal skin, keloids show more frequent hypomethylation but less frequent hypermethylation in the cytosine?phosphodiester bond?guanine(CpG)islands in the whole genome as well as in related DNA promoter regions. Additionally, promoter hypermethylation usually occurs at the same location within susceptibility genes, and act as an early ? stage biomarker. Obviously increased expression and activity of deacetylases can lead to a decrease in histone acetylation and cell apoptosis rate,which finally promote the development of keloids. In keloids, the expression of 23 miRNAs including miR?21 is up?regulated, while that of 9 miRNAs including miR?203 is down?regulated. The role of epigenetic pathway in the formation and development of keloids deserves further study.