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. 2024 Sep 12;15:7638. doi: 10.1038/s41467-024-52068-0

Fig. 3. PKN1 and PKN2 deletion in cardiac fibroblasts suppresses cardiac fibrosis after myocardial infarction.

Fig. 3

a, b Fibrotic changes in the left ventricles after 7 days of myocardial infarction (MI) with the ischemia-reperfusion (IR) model were assessed using Picrosirius red staining (n = 8, biological replicates per group). ns, not significant; ****p < 0.0001. c–e Echocardiogram analysis of left ventricular end-diastolic diameter (d; LVDd) and fractional shortening (e) was performed before and 7 days after MI accompanied by IR (n = 8, biological replicates per group). ns, not significant; ***p = 0.0004; ****p < 0.0001. Fibrotic changes in the left ventricles (f), LVDd (g), and fractional shortening (h) were examined after 28 days of MI with the IR model. ns, not significant; ***p = 0.0005; ****p < 0.0001. i Number of events during 7 days of MI accompanied by permanent ligation of the left coronary artery (n = 15, biological replicates per group). j Fractional shortening 7 days after permanent ligation of the left coronary artery (n = 6, biological replicates per group). ns, not significant; *p = 0.0108; ****p < 0.0001. Data are presented as the mean ± SEM and analyzed using the two-way ANOVA followed by Tukey’s post hoc test (b, d–h, j). The data represent three independent experiments with similar results. Source data are provided as a Source Data file.