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. Author manuscript; available in PMC: 2023 Apr 1.
Published in final edited form as: J Cell Physiol. 2022 Jan 30;237(4):2220–2229. doi: 10.1002/jcp.30687

Figure 4.

Figure 4.

Interactive model of TGF-β, IGF, PAPP-A and cellular senescence in IPF

(A) TGF-β-induced IGF signaling in early stages of fibrosis through increases in IGF-I and PAPP-A expression promotes proliferation and survival of myofibroblasts, the major producer of ECM.

(B) Senescence markedly augments PAPP-A expression and activity in lung SASP while TGF-β-induced expression of IGF-I is retained. Thus, TGF-β, IGF, PAPP-A and senescence appear to interact to promote a pro-fibrotic, anti-apoptotic environment, which could contribute to unresolved pulmonary fibrosis in IPF. In addition, active PAPP-A associated with EVs that are produced by senescent lung fibroblasts and released into the surrounding environment has the potential to participate in crosstalk with other cells in the lung.