Fibrosis—the tale of H3K27 histone methyltransferases and demethylases

Fibrosis, or excessive scarring, is characterized by the emergence of alpha-smooth muscle actin (αSMA)-expressing myofibroblasts and accumulation fibrotic extracellular matrix (ECM). Currently, there a lack effective treatment options for fibrosis, highlighting an unmet need to identify new therapeutic targets. The acquisition phenotype associated with changes in chromatin structure, key determinant gene transcription activation repression. major repressive histone mark, H3K27me3, has been linked dynamic expression fibrosis through alterations structure. H3K27-specific homologous methylase (HMT) enzymes, Enhancer zeste 1 2 (EZH1, EZH2), which are alternative subunits Polycomb Repressive Complex (PRC2) demethylase (KDM) Ubiquitously transcribed tetratricopeptide repeat, X chromosome (UTX), Lysine 6B (KDM6B), responsible regulating methylation status H3K27me3. In this review, we explore how these enzymes regulate structure alter them as attractive targets fibrosis.