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ER stress modulates the function and phenotype of profibrotic cells during the development of pulmonary fibrosis. This schematic paradigm demonstrates how ER stress modulates the function and phenotype of profibrotic cells contributing to IPF pathogenesis. It is believed that ER stress can drive alveolar epithelial cell apoptosis, epithelial-to-mesenchymal transition (EMT), macrophages polarization, and (myo)fibroblasts activation, by which it promotes pulmonary fibrosis.
