Paraquat (PQ) is a highly toxic herbicide that causes fatal pulmonary fibrosis in humans. The molecular mechanisms responsible for PQ-induced pulmonary fibrosis are still not clear, but the epithelial-mesenchymal transition (EMT) has been postulated to be one of the main mechanisms. EMT involves epithelial cell transformation into cells with mesenchymal phenotypes. A growing body of experimental evidence indicates that PQ exposure can induce phenotypes that are characteristic of EMT, including a reduction in the epithelial cell markers E-cadherin and zona occludens 1 (ZO-1), and an increase in the mesenchymal cell markers vimentin and α-smooth muscle actin (α-SMA). In this review, we summarize in vivo and in vitro studies on PQ-mediated pulmonary fibrosis, and discuss the possible involvement of signaling pathways such as transforming growth factor-β1 (TGF-β1)/Smad, Wnt/β-catenin, Notch, and hypoxia-inducible factor 1α (HIF-1α) in regulating pulmonary EMT following exposure to PQ.
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