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研究进步在表观遗传修饰和后翻译修饰在内皮-介质细胞过渡的研究进步

Zhongjun Shen^1,2,3, Shuo Yang^2,3, Qian Zhang^2,3

¹Institute of Medical Technology, Peking University Health Science Center, Beijing, China.

Epigenetics & chromatin

|December 11, 2025

概括

内皮细胞-介质细胞过渡 (EndMT) 涉及细胞从内皮细胞转变为介质细胞类型,影响各种疾病. 表观遗传和翻译后修改通过关键途径和转录因子对EndMT进行了批判性调节.

科学领域:

细胞生物学细胞生物学
分子生物学分子生物学
病理生理学病理生理学

背景情况:

内皮细胞-介质细胞过渡 (EndMT) 是一种过程,其中内皮细胞获得介质细胞特征.
终端MT与心脏发育,纤维化,瘤转移和动脉样硬化有关.
表观遗传和翻译后修饰越来越被认为是EndMT的关键调节者.

研究的目的:

系统地审查表观遗传和后翻译修改在EndMT中的调控作用.
阐明这些修改如何影响关键信号通路和参与EndMT的转录因子.
突出针对EndMT的新型诊断生物标志物和治疗策略的潜力.

主要方法:

对EndMT调节研究的文献综述.
对表观遗传机制的分析:DNA甲基化,基因素修饰,非编码RNAs.
对翻译后修改的分析:酸化,乙化,无处不在化.
对EndMT相关的信号通路 (TGF-β,Wnt,Notch) 和转录因子 (Snail,Slug,Twist,ZEB1/2) 的检查.

主要成果:

表观遗传修饰 (DNA甲基化,基因组模式,ncRNAs) 微调 EndMT.
翻译后的修改 (酸化,乙化,无化) 控制了EndMT的进展.
这些修改调节了EndMT的关键信号通路和转录因子.
具体的例子包括通过TGF-β,Wnt,Notch途径和Snail,Slug,Twist,ZEB1/2因子进行调节.

结论:

表观遗传和翻译后修改是EndMT的关键调节者.
了解这些调节网络,可以深入了解疾病机制.
这些知识可能会导致新的诊断生物标志物和EndMT相关疾病的治疗方法.

关键词:

通过DNA甲基化.内皮细胞-介质细胞过渡.表观遗传修饰表观遗传修饰表观遗传修饰基质子的修改基质子的修改没有编码的RNA.后翻译修改后的修改.

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