Role of epigenetics and miRNAs in orofacial clefts.

Role of epigenetics and miRNAs in orofacial clefts.
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DOI:
10.1002/bdr2.1802
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发表时间:
2020-11
影响因子:
2.1
通讯作者:
Zhou CJ
Zhou CJ
中科院分区:
医学4区
文献类型:
--
作者:
Garland MA;Sun B;Zhang S;Reynolds K;Ji Y;Zhou CJ

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口面裂(OFCs)有多种病因,可能是遗传和环境因素相互作用的结果。在过去的十年中,研究表明特定的表观遗传修饰和非编码RNA作为OFC病因的额外方面。通过DNA甲基化和组蛋白修饰改变的基因表达为特定基因如何促成不同的OFC亚型提供了新的见解。表观遗传学研究也提供了进一步的证据,唇腭裂(CLO)是一个独特的病因学裂亚型。编码microRNA的基因的多态性或错误表达,以及它们的靶点,有助于OFC的风险。在斑马鱼、非洲爪蟾、小鼠和大鼠等动物模型中实验性操纵表观遗传变化和非编码RNA的能力,为各种OFC亚型的机制提供了新的见解。尽管仍有许多问题有待解决,但我们对眶额肌纤维瘤病因学认识的最新进展可能为今后的研究和预防保健提供建议。
Orofacial clefts (OFCs) have multiple etiologies and likely result from an interplay between genetic and environmental factors. Within the last decade, studies have implicated specific epigenetic modifications and non-coding RNAs as additional facets of OFC etiology. Altered gene expression through DNA methylation and histone modification offer novel insights into how specific genes contribute to distinct OFC subtypes. Epigenetics research has also provided further evidence that cleft lip only (CLO) is a cleft subtype with distinct etiology. Polymorphisms or misexpression of genes encoding microRNAs, as well as their targets, contribute to OFC risk. The ability to experimentally manipulate epigenetic changes and non-coding RNAs in animal models, such as zebrafish, Xenopus, mice, and rats, has offered novel insights into the mechanisms of various OFC subtypes. Although much remains to be understood, recent advancements in our understanding of OFC etiology may advise future strategies of research and preventive care.
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