Extended Data Fig. 9: GR transient inhibition facilitates cardiomyocyte proliferation and heart repair in the mouse model.

Schematic diagram showing the role of GR in controlling postnatal cardiomyocyte proliferation and heart regenerative ability. Cardiac GR abundance physiologically increases in cardiomyocytes during the first week of postnatal life (red line) and endogenous glucocorticoids/GR axis in cardiomyocytes contributes to the maturation of myofibrils-mitochondria organization coupled with a metabolic rewiring from glucose catabolism to fatty acid oxidation, in turn resulting in cardiomyocyte cell cycle exit and loss of cardiac regenerative ability. Transient inhibition of GR in adulthood facilitates cardiomyocyte proliferation and heart repair after damage.