Fig. 8: HIF1α mediates Foxk1 and Foxk2-dependent cardiomyocyte metabolic reprogramming.

A FOXK1 and FOXK2 CUT&Tag signal (normalized reads) in the Hif1α locus. Filled boxes indicate peaks. B ChIP-qPCR illustrating the specific binding of FOXK1 and FOXK2 to the Hif1α promoter region (n = 3 per group). C qRT-PCR analysis of the mRNA levels of Hif1α in neonatal cardiomyocytes from Foxk1- or Foxk2-overexpressing and Foxk1- or Foxk2-knockdown cardiomyocytes (n = 4 per group). D Western blot analysis of HIF1α in cardiomyocytes following overexpression and knockdown Foxk1 or Foxk2 (n = 3 per group). E–H Seahorse analysis of glycolytic capacity (E, F) and maximal respiration (G, H) of cardiomyocytes with the indicated treatment (n = 5 per group). I, Quantitative analysis of the percentage of Ki67⁺ cardiomyocytes in the indicated groups (n = 4 for Ad-Ctrl+siHif1α group and n = 3 for other groups). J Immunostaining and quantitative analysis of pH3⁺ cardiomyocytes (green, yellow arrows) in the indicated groups (n = 3 per group). Data are presented as mean ± SEM. p values were determined by two-tailed unpaired t-test (B) and one-way ANOVA with Bonferroni multiple comparisons test (C, E–J). Source data are provided as a Source Data file.