Fig. 1.

HDAC inhibitors attenuate STAT3-mediated fibrosis. HDAC activity is required for STAT3 phosphorylation at tyrosine 705 and dimerization (activation). The dimerized STAT3 is translocated into the nucleus, where it regulates transcription of the target genes associated with development of tissue fibrosis, such as α-smooth muscle actin, fibronectin, and collagen I. HDAC inhibitors such as TSA can inhibit these actions of STAT3 and subsequently attenuate its effects in association of fibrosis.