The Conway Institute, School of Medicine and Medical Science, University College Dublin, Dublin, Ireland.
Epigenetics. 2012 Sep;7(9):987-93. doi: 10.4161/epi.21567. Epub 2012 Aug 16.
Fibrosis of any tissue is characterized by excessive extracellular matrix accumulation that ultimately destroys tissue architecture and eventually abolishes normal organ function. Although much research has focused on the mechanisms underlying disease pathogenesis, there are still no effective antifibrotic therapies that can reverse, stop or delay the formation of scar tissue in most fibrotic organs. As fibrosis can be described as an aberrant wound healing response, a recent hypothesis suggests that the cells involved in this process gain an altered heritable phenotype that promotes excessive fibrotic tissue accumulation. This article will review the most recent observations in a newly emerging field that links epigenetic modifications to the pathogenesis of fibrosis. Specifically, the roles of DNA methylation and histone modifications in fibrotic disease will be discussed.
任何组织的纤维化都以细胞外基质的过度积累为特征，最终破坏组织的结构，并最终导致正常器官功能的丧失。尽管许多研究都集中在疾病发病机制的机制上，但目前仍然没有有效的抗纤维化疗法可以逆转、阻止或延缓大多数纤维化器官中瘢痕组织的形成。由于纤维化可以被描述为异常的伤口愈合反应，最近的一个假说表明，参与这个过程的细胞获得了一种改变的可遗传表型，从而促进了过多的纤维化组织的积累。本文将综述这一新兴领域的最新观察结果，该领域将表观遗传修饰与纤维化的发病机制联系起来。具体来说，将讨论 DNA 甲基化和组蛋白修饰在纤维化疾病中的作用。
