However, we confirmed that BMSCs overexpressing FoxM1 protected against ALI by attenuating pulmonary edema and fibrosis, reducing levels of MDA and inflammatory factors (such as IL-1β, IL-6, IL-8, MIP-1α, and TGF-β), and increasing the level of SOD, indicating that the therapeutic effects of FoxM1-overexpressing BMSCs might be attributed to paracrine mechanisms. Here, TGFB1 is linked to acute respiratory distress syndrome.