Fig. 9: Schematic depicting HDAC9-mediated epithelial cell cycle arrest in G2/M contributes to kidney fibrosis. | Nature Communications

Fig. 9: Schematic depicting HDAC9-mediated epithelial cell cycle arrest in G2/M contributes to kidney fibrosis.

From: HDAC9-mediated epithelial cell cycle arrest in G2/M contributes to kidney fibrosis in male mice

Fig. 9: Schematic depicting HDAC9-mediated epithelial cell cycle arrest in G2/M contributes to kidney fibrosis.The alternative text for this image may have been generated using AI.

In pathological condition, HDAC9 contributes to G2/M arrest in tubular epithelial cells by regulating the activation of STAT1, followed by inducing production of profibrotic cytokine, such as TGF-β1, which promoted the loss of epithelial phenotype in tubular epithelial cells and activation of fibroblasts evidenced by upregulation of profibrotic genes, finally causing kidney tubulointerstitial fibrosis. HDAC9 histone deacetylase 9, STAT1 signal transducer and activator of transcription 1, p21 cyclin-dependent kinase inhibitor p21, G2 G2 phase of the cell cycle, M M phase of the cell cycle, G1 G1 phase of the cell cycle, S S phase of the cell cycle, TGF-β1 transforming growth factor β1, CTGF connective tissue growth factor.

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