ACTA1 and pulmonary fibrosis: To determine the role of fibroblast HIF-α in pulmonary fibrosis, Goodwin et al. examined fibroblasts derived from bleomycin-induced pulmonary fibrosis animal models and showed that hypoxia significantly enhanced TGF-β-induced myofibroblast differentiation and α-SMA expression through HIF-1α [43].