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Epigenetic regulation of wound healing and fibrosis

机译:伤口愈合和纤维化的表观遗传调控

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Purpose of Review: Wound healing is a normal physiological response to tissue injury which can occur in any organ. Mechanisms that orchestrate wound healing in different organs are surprisingly generic, involving generation of fibroblasts and myofibroblasts by differentiation processes that require extensive alterations in gene expression. This process and indeed phenotype of cells are orchestrated by the combined influences of molecular components of epigenome including DNA methylation, vast array of posttranslational modifications of the histone protein constituents of chromatin and regulatory noncoding RNAs of which microRNAs (miRs) are the most extensively studied. Recent Findings: Numerous studies from the last 12 months show all the three epigenetic mechanisms to be regulating generation and apoptosis of myofibroblasts in organs affected by perturbed wound healing. Furthermore, these mechanisms are involved in fibrotic disease itself, with some miRs and epigenetic drugs being tested for their therapeutic potential. Summary: Fields of wound healing and fibrosis will be enriched over the next decade by plethora of new information regarding epigenetic control mechanisms which will hopefully provide new advances in diagnostics and prognostics. With the design of ever more specific epigenetic drugs, we may improve our ability to therapeutically optimize wound healing and prevent fibrosis in chronic disease and ageing.
机译:审查目的:伤口愈合是对任何器官可能发生的组织损伤的正常生理反应。协调不同器官伤口愈合的机制令人惊讶地通用,涉及通过分化过程产生成纤维细胞和成肌纤维细胞,而分化过程需要基因表达的大量改变。表观基因组的分子成分包括DNA甲基化,染色质的组蛋白成分的翻译后修饰修饰以及调控性非编码RNA的综合影响共同协调了这一过程以及细胞的表型,其中对microRNA(miRs)的研究最为广泛。最近的发现:最近12个月的大量研究表明,这三种表观遗传机制均在调节受创伤口愈合影响的器官中成肌纤维细胞的生成和凋亡。此外,这些机制与纤维化疾病本身有关,一些miRs和表观遗传药物正在测试其治疗潜力。简介:在未来十年中,伤口愈合和纤维化的领域将通过关于表观遗传控制机制的大量新信息得以丰富,有望为诊断和预后研究提供新的进展。通过设计越来越特殊的表观遗传药物,我们可以提高治疗能力,以优化伤口愈合并预防慢性疾病和衰老中的纤维化。

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