TGFB1 and pulmonary fibrosis: Their results suggested that miR-26a expression level was decreased through TGF-β1-mediated phosphorylation of Smad3, and its over-expression could repress the fibrotic process (77), (5) another study indicated that miR-486-5p over-expression substantially attenuated lung injury severity and its dissemination in mice with BLM- or silica-induced lung fibrosis (78).