DNA methylation regulated gene expression in organ fibrosis
DNA methylation regulated gene expression in organ fibrosis
复制标题
DNA甲基化调节器官组织中的基因表达
DOI：
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发表时间：
2017
期刊：
影响因子：
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通讯作者：
ers
中科院分区：
文献类型：
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作者：
张湘瑜;胡敏;吕星;李纯;Yan Y. S;ers
DNA甲基化是调节基因表达的主要表观遗传机制。多个有助于显着的发病率和异常的DNA甲基化的器官，可以激活纤维化的基因表达模式。器官，包括心脏和肺部，具有有限的治疗选择，例如其他表观遗传学过程，因此被视为有吸引力的治疗性干预措施。抗纤维化基因和有机纤维中DNA甲基化调节的途径；
DNA methylation is a major epigenetic mechanism to regulate gene expression. Epigenetic regulation, including DNA methylation, histone modifications and RNA interference, results in heritable changes in gene expression independent of alterations in DNA sequence. Epigenetic regulation often occurs in response to aging and environment stimuli, including exposures and diet. Studies have shown that DNA methylation is critical in the pathogenesis of fibrosis involving multiple organ systems, contributing to significant morbidity and mortality. Aberrant DNA methylation can silence or activate gene expression patterns that drive the fibrosis process. Fibrosis is a pathological wound healing process in response to chronic injury. It is characterized by excessive extracellular matrix production and accumulation, which eventually affects organ architecture and results in organ failure. Fibrosis can affect a wide range of organs, including the heart and lungs, and have limited therapeutic options. DNA methylation, like other epigenetic process, is reversible, therefore regarded as attractive therapeutic interventions. Although epigenetic mechanisms are highly interactive and often reinforcing, this review discusses DNA methylation-dependent mechanisms in the pathogenesis of organ fibrosis, with focus on cardiac and pulmonary fibrosis. We discuss specific pro- and anti-fibrotic genes and pathways regulated by DNA methylation in organ fibrosis; we further highlight the potential benefits and side-effects of epigenetic therapies in fibrotic disorders.