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. 2023 Jan 31;91(1):26–48. doi: 10.3390/arm91010005

Figure 1.

Figure 1

Pathological changes in idiopathic pulmonary fibrosis. (A) Normally, various cells in the lung work in their own right and work together to maintain lung function and function properly. (B) When the lung is exposed to risk factors (e.g., cigarette smoke, genetic or epigenetic alterations, aging) that cause repeated microdamage to the lung epithelium, inadequate metaplasia of epithelial cells, disruption of the basement membrane, and imbalances in lung homeostasis, the balance between lung and other environmental insults occurs. Aberrant vascular remodeling, epithelial–mesenchymal crosstalk, fibroblast dysplasia, immune attenuation, provocation of profibrotic mediators, activation of fibrotic pathways, deposition of extracellular matrix, and formation of fibrotic foci are induced in this setting. Abbreviations: AT1, alveolar type I epithelial cells; AT2, alveolar type II epithelial cells; ADI, alveolar differentiation intermediate; MSC, mesenchymal stem cells; EC, endothelial cells; ER, endoplasmic reticulum; TGF-β, transforming growth factor-β; ECM, extracellular matrix; EMT, epithelial–mesenchymal transformation; EndMT, endothelial–mesenchymal transition; VEGF, vascular endothelial growth factor.