Hiltunen Mikko O, Ylä-Herttuala Seppo
A.I. Virtanen Institute, University of Kuopio, Kuopio, Finland.
Arterioscler Thromb Vasc Biol. 2003 Oct 1;23(10):1750-3. doi: 10.1161/01.ATV.0000092871.30563.41. Epub 2003 Aug 28.
DNA methylation is a form of epigenetic modification of the genome that can regulate gene expression. Hypermethylation of CpG islands in the promoter areas leads to decreased gene expression, whereas promoters of actively transcribed genes remain nonmethylated. Because of cellular proliferation and monoclonality of at least some of the lesion cells, atherosclerotic lesions have been compared with benign vascular tumors.1,2 However, although genetic and epigenetic background favors neoplastic transformation, atherosclerotic plaques never develop to malignant tumors. Among cancer cells, common features are genome-wide hypomethylation, which correlates with transformation and tumor progression. Recent studies have shown that DNA methylation changes occur also during atherogenesis and may contribute to the lesion development.
DNA甲基化是基因组表观遗传修饰的一种形式，可调控基因表达。启动子区域CpG岛的高甲基化会导致基因表达降低，而活跃转录基因的启动子则保持非甲基化状态。由于至少部分病变细胞具有细胞增殖和单克隆性，动脉粥样硬化病变已被与良性血管肿瘤相比较。然而，尽管遗传和表观遗传背景有利于肿瘤转化，但动脉粥样硬化斑块从未发展为恶性肿瘤。在癌细胞中，常见特征是全基因组低甲基化，这与转化和肿瘤进展相关。最近的研究表明，DNA甲基化变化在动脉粥样硬化形成过程中也会发生，并且可能有助于病变发展。
