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首页> 外文期刊>Cellular Signalling >The epigenetic feedback loop between DNA methylation and microRNAs in fibrotic disease with an emphasis on DNA methyltransferases
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The epigenetic feedback loop between DNA methylation and microRNAs in fibrotic disease with an emphasis on DNA methyltransferases

机译：纤维化疾病中DNA甲基化与microRNA之间的表观遗传反馈回路，重点是DNA甲基转移酶

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Epigenetic processes play a key regulatory role in many cancers. Recently, it also has been demonstrated to participate in fibrogenesis, especially in fibrotic disease. Fibrotic disease is a pathological response to tissue injury which can occur in any organ. Mechanisms that orchestrate fibrotic disorders in different organs are amazingly generic, involving generation of activated fibroblasts and myofibroblasts by differentiation processes that require extensive alterations in gene expression. Apart from genetic and environmental factors, epigenetic modifications including a combination of microRNAs and DNA methylation are supposed as regulatory mechanisms to control myofibroblast differentiation. It has become obvious that microRNAs, which act as regulators of gene expression at a post-transcriptional level, are differentially expressed in differentiating cells and play important roles in governing DNA methyltransferases (DNMTs) which are enzymes responsible for setting up and maintaining DNA methylation patterns at specific regions of the genome. Some microRNAs targeting DNMT transcripts lead to the demethylation and transcriptional activation of numerous protein coding gene sequences, thereby contributing to gene expression. Moreover, DNMTs also have a critical role in controlling some specific microRNA expression. This cooperative action among DNMTs, microRNAs and DNA methylation indicates that DNMTs may participate in the pathogenesis of myofibroblast differentiation through silencing of certain gene transcription. In this review, we summarize the current knowledge of a potential link between microRNA expression and DNA methylation on how DNMTs work in the process of fibrogenesis.
机译：表观遗传过程在许多癌症中起着关键的调节作用。最近，也已证明其参与纤维发生，尤其是纤维变性疾病。纤维化疾病是对任何组织中可能发生的组织损伤的病理反应。协调不同器官中纤维化疾病的机制非常普遍，涉及通过分化过程产生活化的成纤维细胞和成肌纤维细胞，而这种分化过程需要基因表达的大量改变。除了遗传和环境因素外，表观遗传修饰（包括microRNA和DNA甲基化的组合）被认为是控制成肌纤维细胞分化的调节机制。很明显，在转录后水平上充当基因表达调节剂的microRNA在分化细胞中差异表达，并在调控DNA甲基转移酶（DNMT）中起重要作用，DNMT是负责建立和维持DNA甲基化模式的酶在基因组的特定区域。一些靶向DNMT转录本的microRNA导致许多蛋白质编码基因序列的去甲基化和转录激活，从而有助于基因表达。此外，DNMT在控制某些特定的microRNA表达中也起着关键作用。 DNMT，microRNA和DNA甲基化之间的这种协同作用表明DNMT可能通过沉默某些基因转录而参与成肌纤维细胞分化的发病机制。在这篇综述中，我们总结了DNMT在纤维发生过程中如何工作的microRNA表达与DNA甲基化之间潜在联系的最新知识。

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