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Fig. 8 | Clinical Epigenetics

Fig. 8

From: Histone deacetylase 3 deletion in alveolar type 2 epithelial cells prevents bleomycin-induced pulmonary fibrosis

Fig. 8

Schematic illustration of the mechanisms of HDAC3 in AT2 cells. TGF-β1 expression is upregulated in pulmonary fibrosis and phosphorylates SMAD3 through the TGF-βRI receptor. Activated SMAD3 directly binds to the promoter of HDAC3 to increase its transcription. HDAC3 further decreases the acetylation of GATA3 and inhibits its degradation, which promotes the epithelial-mesenchymal transition of AT2 cells by decreasing E-cadherin expression and increasing expression of N-cadherin and vimentin, which aggravates pulmonary fibrosis

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Clinical Epigenetics

ISSN: 1868-7083

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