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Updated: Jul 26, 2025

TGF-β-mediated Endothelial to Mesenchymal Transition EndMT and the Functional Assessment of EndMT Effectors using CRISPR/Cas9 Gene Editing
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TGF-β-mediated Endothelial to Mesenchymal Transition EndMT and the Functional Assessment of EndMT Effectors using CRISPR/Cas9 Gene Editing

Published on: February 26, 2021

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恩多林-1通过破坏HDAC2/Sin3A/MeCP2核心压缩复合体来诱导人类肺纤维细胞中的结合组织生长因子表达

Hung-Sheng Hua1, Heng-Ching Wen1, Hong-Sheng Lee1,2

  • 1Graduate Institute of Medical Sciences, College of Medicine, Taipei Medical University, 250 Wu-Hsing Street, Taipei, 110, Taiwan.

Journal of biomedical science
|June 13, 2023
PubMed
概括

HDAC2/Sin3A/MeCP2复合物抑制CTGF,这是气道纤维化的一个关键因素. 这种复杂的干扰促进了CTGF的产生,突出了HDAC2和Sin3A.

关键词:
气道纤维化 气道纤维化在CTGF中,CTGF是CTGF.在ET-1和ET-1之间.在 HDAC2 中.肺部纤维母细胞 肺部纤维母细胞这就是MeCP2的意义.在 Sin3A 中使用.

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