Karla Rubio, Alejandro Molina-Herrera, Andrea Pérez-González,Hury Viridiana Hernández-Galdámez, Carolina Piña-Vázquez, Tania Araujo-Ramos and Indrabahadur Singh
EP300 as a Molecular Integrator of Fibrotic Transcriptional Programs cancer
Fibrosisis a condition characterized by the excessive accumulation of extra cellular matrix proteins in tissues, leading to organ dysfunction and failure. Recen tstudies have identiﬁed EP300 ,a histone acetyltransferase, as a crucia lregulator of the epigenetic changes that contribute to ﬁbrosis. Infact, EP300-mediated acetylation of histones alters global chromatin structure and gene expression, promoting the development and progression of ﬁbrosis. Here, were view the role of EP300-mediated epigenetic regulation inmulti-organ ﬁbrosis and its potential as a therapeutic target. We discuss the preclinical evidence that suggests that EP300 in hibition can attenuate ﬁbrosis-related molecular processes, including extra cellular matrix deposition, inﬂammation, and epithelial-to-mesenchymal transition. We also highlight the contributions of small molecule in hibitors and gene therapy approaches targeting EP300 as novel therapies against ﬁbrosis.