Fig. 7 | Laboratory Investigation

Fig. 7

From: The Shh/Gli signaling cascade regulates myofibroblastic activation of lung-resident mesenchymal stem cells via the modulation of Wnt10a expression during pulmonary fibrogenesis

Fig. 7

Proposed model for hedgehog-Wnt signaling in the modulation of pulmonary fibrosis. During pulmonary fibrosis, sonic hedgehog (Shh) signaling is activated, and lung-resident mesenchymal stem cells (LR-MSCs) are the responsive cells. Shh interacts with the patched (Ptc) receptor to initiate a series of intracellular events that activate glioblastoma (Gli) factors, which subsequently translocate to the nucleus and promote the transcription of Wnt10a through binding with its promoter. Next, secreted Wnt10a acts on the surrounding LR-MSCs in an autocrine or paracrine manner. In the presence of Wnt10a, low-density lipoprotein receptor-related protein (LRP) forms a complex with Wnt-bound Frizzled (Fzd). Formation of this complex leads to nuclear translocation of active β-catenin, triggering myofibroblastic differentiation of LR-MSCs and pulmonary fibrosis. Accordingly, inhibition of the hedgehog-Wnt signaling can efficiently suppress the pulmonary fibrotic events

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