BRD4 inhibition mitigates acute and chronic corneal injury following topical nitrogen mustard exposure

cells by 86%) and oxidative stress and conferred long-term preservation of corneal clarity, stromal organization, and endothelial integrity. Selective inhibition of BD1 or BD2 recapitulated JQ1's effects, indicating that blockade of either BD is sufficient. BRD4 inhibition also significantly attenuated NM-induced corneal pathology in a rabbit model, supporting cross-species efficacy and translational relevance. Mechanistically, BRD4 inhibition selectively counteracted key NM-driven pathogenic programs, including inflammation, oxidative stress, and extracellular matrix remodeling. These findings identify BRD4 as a central epigenetic driver of vesicant-induced corneal injury and position BRD4 inhibition as a promising translational therapeutic strategy.