Furthermore, a number of reports have proposed that cross-talk between TGFβ and hypoxia may promote fibrosis, with hypoxia and TGFβ1 synergistically increasing myofibroblast marker expression (Senavirathna et al., 2020), promoting experimental nickel oxide nanoparticle-induced lung fibrosis (Qian et al., 2015), and HIF1α mediating TGF-β-induced PAI-1 production in alveolar macrophages in the bleomycin model of lung fibrosis (Ueno et al., 2011). Here, HIF1A is linked to pulmonary fibrosis.