TGFB1 and pulmonary fibrosis: Oxidative stress is considered a crucial molecular mechanism associated with fibrotic diseases, increasing evidence indicates that oxidative stress contributes to the processes of pulmonary fibrosis, including myofibroblast differentiation, alveolar epithelial cell apoptosis, endothelial cell barrier disruption, and elevated expression of transforming growth factor-beta 1 (TGF-β1), promoting fibrosis [7–9].