HDAC9 and acute respiratory distress syndrome: 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.