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. 2022 Dec 27;15(1):186–203. doi: 10.21037/jtd-22-886

Figure 1.

Figure 1

The main mechanism of alveolar epithelial cell senescence in idiopathic pulmonary fibrosis. DNA damage and ROS are essential causes of cycle arrest induced by WNT, PI3K/Akt, NF-κB and mTOR signaling pathways. Changes in lipid metabolism in alveolar epithelial cells can also be induced by mitochondrial dysfunction, both of which contribute to cellular senescence and IPF. NF-κB and mTOR pathways can promote IPF by promoting the secretion of senescence-associated secretory phenotype-associated markers. ROS, reactive oxygen species; IPF, idiopathic pulmonary fibrosis; PI3K/Akt, phosphatidylinositol-3-kinase/protein kinase B; NF-κB, nuclear factor kappa B; mTOR, mammalian target of rapamycin; mtROS, mitochondrial reactive oxygen species; ETC, electron transport chain; mtDNA, mitochondrial DNA; SASP, senescence-associated secretory phenotype; IL, interleukin; MMP, matrix metalloproteinase.