This activation of β-catenin stimulated the proliferation of collagen-producing cells at the ischemic edge and, ultimately, promoted fibrosis.146 Following acute ischemic heart injury, Wnt1 expression is upregulated, which induces the proliferation of cardiac fibroblasts, increases the expression of pro-fibrotic genes by activating Wnt1/β-catenin signaling, and promotes cardiac repair.147 In contrast, inhibition of Wnt1/β-catenin signaling in cardiac fibroblasts can impair cardiac function and ventricular dilatation.147. The gene discussed is WNT1; the disease is Ventriculomegaly.