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Injury to the kidney results in increased expression of HDAC8 in renal tubular cells. Increased HDAC8 activity leads to the activation of TGFβ/Smad3, STAT3, β-catenin signaling, induction of epithelial cells arrested at G2/M phase of cell cycle, upregulation of Snail and downregulation of klotho and BMP-7. Blocking class HDAC8 inhibits all these profibrotic responses.
