Our study demonstrated that using the antifibrotic agent HDAC inhibitor TSA can reduce MV-augmented bleomcyin-induced pulmonary fibrosis by reducing alveolar capillary leakage, oxidative stress, MMP-9 and PAI-1, and total collagen through the inhibition of EMT, and achieve pathological, radiological, and functional improvements in our animal model that mimicked the fibroproliferation in ARDS. This evidence concerns the gene HDAC9 and pulmonary fibrosis.