TGFB1 and pulmonary fibrosis: Alterations of fibrosis-related pathways and mechanisms, such as decreased expression of angiotensin-converting enzyme 2 (ACE2), overexpression of the TGF-β/Smad pathway, increased production of pro-fibrotic and pro-inflammatory cytokines, as well as increased stress in the endoplasmic reticulum, have been shown to contribute to epithelial-mesenchymal transformation, a major mechanism of pulmonary fibrosis (188).