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Fig. 7 | Inflammation and Regeneration

Fig. 7

From: Autocrine insulin-like growth factor 2 signaling as a potential target in the associated development of pulmonary emphysema and cancer in smokers

Fig. 7

Illustration of the summary of the results. Chronic NB treatment induces persistent upregulation of IGF2 expression through NNK/β-AR, NNK/nAchR, and BaP/AhR-mediated signal transduction cascades and facilitates IGF2 exocytosis through nAChR-mediated membrane depolarization and subsequent VDCC-mediated Ca2+ influx. The consequent overactivation of IGF-1R/IR signaling results in the disruption of the stem cell function of AT2s, causing poor recovery of lung architecture against NB-mediated injury and the transformation of normal lung epithelial cells into malignant cells. These overall events ultimately lead to the concurrent development of emphysema and lung cancer. Abrogation of IGF2 availability by using IGF2-specific neutralizing mAbs or blocking VDCC-mediated Ca2+ influx by using CCB alleviates NB-mediated associated development of emphysema or lung cancer

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Inflammation and Regeneration

ISSN: 1880-8190

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