Since sFRP2 was shown to activate Wnt/β-catenin signaling in cardiac fibroblasts and contribute to cardiac extracellular matrix remodeling [146, 147], the strongest inhibitory effect of cotreatment on the expression of sFRP2 was shown to inhibit the Wnt3a/β-catenin pathway in CFs exposed to HG conditions, which was superior in ameliorating fibrosis in cases of DCM [145]. Here, SFRP2 is linked to familial dilated cardiomyopathy.