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. Author manuscript; available in PMC: 2017 Jan 22.
Published in final edited form as: Circ Res. 2016 Jan 22;118(2):296–310. doi: 10.1161/CIRCRESAHA.115.305139

Figure 3. Force-induced modulation of Wnt signaling during cardiomyogenesis.

Figure 3

A, Schematic representation of Wnt signaling cascade and cadherin-based mechanical interactions between adjacent cells. Wnt ligand signaling through its Frizzled receptor inhibits the proteolytic degradation of β-catenin by its destruction complex, enabling cytoplasmic accumulation. Increased cytoplasmic β-catenin drives nuclear translocation and initiates expression of Wnt-related genes to modulate cardiomyogenesis. Cadherins interact with the Wnt pathway by binding β-catenin to block its cytoplasmic accumulation and subsequent nuclear translocation. B, Illustration of epithelial–mesenchymal transition (EMT) driving myocyte specification and migration. The loss of E-cadherin–based mechanical connections between cells enables cell migration and increases intracellular β-catenin pools to drive expression of EMT-related genes. APC indicates adenomatous polyposis coli; GSK3β, glycogen synthase kinase 3 β; LEF, lymphoid enhancer–binding factor; and TCF, transcription factor.