He Yongjing, Deng Zhenjun, Alghamdi Mansour, Lu Lechun, Fear Mark W, He Li
Department of Plastic Surgery, Second Affiliated Hospital of Kunming Medical University, Kunming, China.
Department of Dermatology, First Affiliated Hospital of Kunming Medical University, Kunming, China.
Cell Prolif. 2017 Apr;50(2). doi: 10.1111/cpr.12326. Epub 2017 Jan 5.
Keloid scarring is a dermal fibroproliferative response characterized by excessive and progressive deposition of collagen; aetiology and molecular pathology underlying keloid formation and progression remain unclear. Genetic predisposition is important in the pathogenic processes of keloid formation, however, environmental factors and epigenetic mechanisms may also play pivotal roles. Epigenetic modification is a recent area of investigation in understanding the molecular pathogenesis of keloid scarring and there is increasing evidence that epigenetic changes may play a role in induction and persistent activation of fibroblasts in keloid scars. Here we have reviewed three epigenetic mechanisms: DNA methylation, histone modification and the role of non-coding RNAs. We also review the evidence that these mechanisms may play a role in keloid formation - in future, it may be possible that epigenetic markers may be used instead of prognostic or diagnostic markers here. However, there is a significant amount of work required to increase our current understanding of the role of epigenetic modification in keloid disease.
瘢痕疙瘩是一种真皮纤维增生性反应,其特征是胶原蛋白过度且进行性沉积;瘢痕疙瘩形成和进展的病因及分子病理学仍不清楚。遗传易感性在瘢痕疙瘩形成的致病过程中很重要,然而,环境因素和表观遗传机制也可能起关键作用。表观遗传修饰是理解瘢痕疙瘩分子发病机制的一个新研究领域,越来越多的证据表明,表观遗传变化可能在瘢痕疙瘩中诱导成纤维细胞并使其持续活化。在此,我们综述了三种表观遗传机制:DNA甲基化、组蛋白修饰和非编码RNA的作用。我们还综述了这些机制可能在瘢痕疙瘩形成中发挥作用的证据——未来,在此处可能用表观遗传标记物替代预后或诊断标记物。然而,要增进我们目前对表观遗传修饰在瘢痕疙瘩疾病中作用的理解,仍需要大量工作。