CCL2 and pulmonary fibrosis: In addition to the above pathways, AECs also participate in pulmonary fibrosis through the secretion of a variety of mediators, including growth factor (TGF-β, PDGF/CTGF/IGF-I/insulin-like growth factor binding proteins 3 and 5), matrix metalloproteinases (MMP1/MMP2/MMP7), chemokines (CCL17/CCL2/CXCL12), pigment epithelium-derived factor, autotaxin, sphingosine-1-phosphate, neuregulin (NRG) 1α, growth and differentiation factor 15 (GDF15), transmembrane protease serine 4 (TMPRSS4), tumor necrosis factor-alpha (TNF-α), osteopontin, and angiotensinogen.