Fig. 3: Cardiomyocyte-specific Foxk1 or Foxk2 deficiency impairs heart regeneration.

A Experimental design: Tamoxifen was injected on postnatal day 0 (P0), P1, and P2 to induce Foxk1 or Foxk2 deletion in cardiomyocytes. Myocardial infarction (MI) was induced on P1. Heart tissues were collected at 5- and 28-days post-infarction (dpi), and echocardiography was performed at 28 dpi. B, C Western blot analysis of FOXK1 (B) and FOXK2 (C) expression in the hearts of Foxk1 cKO or Foxk2 cKO mice after tamoxifen injection (n = 3 mice per group). D, E Representative images of Masson staining and quantitative analysis of fibrotic scar size in Foxk1 cKO (D), Foxk2 cKO (E) and the littermate hearts at 28 dpi (n = 8 in Foxk1^fl/fl group, n = 10 in Foxk1 cKO group. n = 11 in Foxk2^fl/fl group, n = 7 in Foxk2 cKO group). F, G WGA staining and quantitative analysis of cardiomyocyte size in Foxk1 cKO (F), Foxk2 cKO (G), and littermate hearts at 28 dpi (n = 6 per group). H–K Representative images and quantitative analysis of pH3⁺ and Aurora B⁺ cardiomyocytes (green, indicated by yellow arrows) in Foxk1 cKO (H, J), Foxk2 cKO (I, K), and littermate hearts at 5 dpi (n = 3 per group) from the border zone. L, M Representative echocardiography images and quantification of ejection fraction and fractional shortening in Foxk1 cKO (L), Foxk2 cKO (M) and littermate hearts at 28 dpi (n = 9 in Foxk1^fl/fl group, n = 11 in Foxk1 cKO group. n = 9 in Foxk2^fl/fl group, n = 7 in Foxk2 cKO group). Data are presented as mean ± SEM. p values were determined by two-tailed unpaired t-tests (D–G, L, and M) and two-way ANOVA with Bonferroni multiple comparisons test (H–K). Source data are provided as a Source Data file.