Epigenetic regulation in fibrosis progress
Epigenetic regulation in fibrosis progress
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纤维化进展中的表观遗传调控
DOI：
10.1016/j.phrs.2021.105910
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发表时间：
2021-10-01
影响因子：
9.3
通讯作者：
Ye, Tinghong
中科院分区：
文献类型：
--
作者：
Xue, Taixiong;Qiu, Xingyu;Ye, Tinghong
纤维化是慢性炎症性疾病的常见过程，被定义为当器官经历持续损伤时的修复反应障碍，最终导致瘢痕形成和功能衰竭。在世界范围内，纤维化疾病导致高死亡率，不幸的是，在临床实践中的治疗手段有限。随着深度测序技术的发展和应用，全面探索纤维化的表观遗传机制成为可能。随后证实了表观遗传学控制各种细胞表型和参与纤维化的分子机制的广泛重塑。本文综述了DNA甲基化、组蛋白修饰、非编码RNA（ncRNA）和N6-甲基腺苷（m6 A）修饰在器官纤维化中的调节机制，重点介绍了心脏、肝脏、肺和肾脏。此外，我们强调表观遗传学在纤维化相关的细胞和分子机制的多样性。最后，对基于表观遗传学的靶向治疗肝纤维化的潜力和前景进行了展望。
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.