Fig. 2.

Histone modification and DNA methylation in kidney fibrosis. Suppression of antifibrotic genes (e.g., RASAL1, KLOTHO, KLF4, Smad7) could be accomplished by DNA methyltransferase (DNMT)-governed DNA methylation, HDACs-induced deacetylation, and histone methyltransferase (HMT)-driven methylation (e.g., H3K9me, H3K27me). On the contrary, HATs-mediated histone acetylation, HMT-ruled H3K4me, and BET proteins are involved in profibrotic gene transcriptional activation (TGF-β, Smad3, α-SMA, Snail, Twist, STAT3, et al.) α-SMA alpha-smooth-muscle actin, BMP-7 bone morphogenic protein 7, BRD4 bromodomain-containing protein 4, Col1a collagen-1α, KLF4 Krüppel-like factor 4, RASAL1 RAS protein activator like 1, SFRP5 secreted frizzled-related proteins 5, STAT3 signal transducer and activator of transcription 3, TGF-β transforming growth factor beta