fig4

Pharmacological suppression of the WNT signaling pathway attenuates age-dependent expression of the phenotype in a mouse model of arrhythmogenic cardiomyopathy

Figure 4. Effects of suppression of the cWNT pathway on the transcript levels of selected genes involved in myocardial fibrosis. Transcript levels of several genes involved in myocardial fibrosis were quantified by RT-PCR in the experimental groups (N = 5 to 7 mice per group). Treatment with WNT974 suppressed and normalized transcript levels of the majority of the pro-fibrotic genes that were upregulated in Myh6-Cre:DspW/F mouse hearts. Tgfb: transforming growth factor β; Postn: periostin; Pcolce: procollagen C-endopeptidase enhancer; Pdgfra: platelet derived growth factor α; Col1a1, Col3a1, and Col6a3: collagen 1α1, collagen 3α, and collagen 6α3, respectively; Timp1: tissue inhibitor of metalloproteinase 1; MMP2: matrix metallopeptidase 2; Gdf15: growth differentiation factor 15. PG: P value for the effect of the genotype; PTr: P value for the effect of treatment; Pi: P value for treatment-by-genotype interaction.

The Journal of Cardiovascular Aging

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