表观遗传学
纤维化
DNA甲基化
组蛋白
生物
癌症研究
后生
生物信息学
肺纤维化
表型
计算生物学
医学
遗传学
病理
DNA
基因
基因表达
作者
Taixiong Xue,Xingyu Qiu,Hongyao Liu,Cailing Gan,Zui Tan,Yuting Xie,Di Wang,Tinghong Ye
标识
DOI:10.1016/j.phrs.2021.105910
摘要
Fibrosis, a common process of chronic inflammatory diseases, is defined as a repair response disorder when organs undergo continuous damage, ultimately leading to scar formation and functional failure. Around the world, fibrotic diseases cause high mortality, unfortunately, with limited treatment means in clinical practice. With the development and application of deep sequencing technology, comprehensively exploring the epigenetic mechanism in fibrosis has been allowed. Extensive remodeling of epigenetics controlling various cells phenotype and molecular mechanisms involved in fibrogenesis was subsequently verified. In this review, we summarize the regulatory mechanisms of DNA methylation, histone modification, noncoding RNAs (ncRNAs) and N6-methyladenosine (m6A) modification in organ fibrosis, focusing on heart, liver, lung and kidney. Additionally, we emphasize the diversity of epigenetics in the cellular and molecular mechanisms related to fibrosis. Finally, the potential and prospect of targeted therapy for fibrosis based on epigenetic is discussed.
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