“…In the early period of PF, the affected lungs are mainly inflammatory cell infiltration, edema and congestion, and then converted to the injury of alveolar epithelial cells (AEC), abnormal proliferation of ECM-producing cells (mesenchymal cells including fibroblasts (FB) and myofibroblasts (MFb)), the overproduction of ECM (collagens, laminin, tenascin-C, etc. ), resulting in progressive scarring and loss of lung function (Rajasekaran et al, 2015;Li et al, 2015a;Craig et al, 2015). Up to now, lots of studies have shown that the molecular mechanisms of PF is involved in the superabundant inflammation such as cytokines release and inflammasome activation (Hosseinian et al, 2015), macrophages activation , FB to MFb transformation (Wollin et al, 2014), epithelial-mesenchymal transition (EMT, converting from epithelial phenotype to fibroblastic phenotype) , matrix metalloproteinase (MMP)/(tissue inhibitor of metalloproteinase (TIMP)) balance , oxidative stress (Brass et al, 2016) and several signaling pathways activation (Chaudhary et al, 2007;Chen et al, 2016b) (Fig.…”