Fig. 9: PKN1/2 deletion suppressed the differentiation of cardiac fibroblasts in the HFpEF model.

a Immunofluorescent staining of fibroblasts and myofibroblasts at 10 weeks after combination exposure to HFD and L-NAME in Pdgfra-PKN1/2 WT and KO male mice (red, vimentin; green, αSMA; blue, nuclei). b Quantification of dual-positive cells for vimentin and αSMA shown as a percentage of vimentin-positive cells (n = 6, biological replicates per group). ns, not significant; ***p = 0.0008; ****p < 0.0001. c Quantification of the number of cardiac fibroblasts with phosphorylated Smad3 (Ser423/425) at 10 weeks after combination exposure to HFD and L-NAME in Pdgfra-PKN1/2 WT and KO male mice (n = 6, biological replicates per group). ns, not significant; ****p < 0.0001. Immunofluorescent images (d) and quantification of the number (e) of cardiac fibroblasts with phosphorylated p38 at 10 weeks after combination exposure to HFD and L-NAME in Pdgfra-PKN1/2 WT and KO male mice (n = 6, biological replicates per group. Red, Pdgfra; green, phosphorylated p38; blue, nuclei). ns, not significant; ****p < 0.0001. f Schematic diagram showing PKN1/2-mediated cardiac fibrosis. Data are presented as the mean ± SEM and analyzed using two-way ANOVA followed by the Tukey’s post hoc test (b, c, e). The data represent three independent experiments with similar results. Source data are provided as a Source Data file.