Distinct Roles of Wnt/β-Catenin Signaling in the Pathogenesis of Chronic Obstructive Pulmonary Disease and Idiopathic Pulmonary Fibrosis

Figure 2

Scheme of possibly distinct pathogenic role of Wnt/β-catenin signaling in COPD and IPF. Possible mechanisms of Wnt/β-catenin signaling in the pathogenesis of COPD (right) and IPF (left) are proposed based on the literatures. In IPF, an enhanced Wnt/β-catenin signaling of epithelial cells interacts with TGF-β to promote EMT, which leads to mesenchymal overgrowth and fibrosis. On the other hand, activated Wnt signaling can increase the expression of Wnt target genes related to cell proliferation and ECM, which leads to bronchiolar overgrowth and honeycombing. In the case of COPD, a decreased Wnt/β-catenin signaling activity in the mesenchymal compartment results in the reduced expression of Wnt target genes related to cell proliferation, leading to mesenchymal deficiency and the reduction of ECM protein expression in alveolar cells, accordingly the development of emphysema or dysfunctions MSCs and immune regulations in small airway, which leads to enhance inflammation in airway.