The neonatal myeloid hypoxia response promotes cardiac regeneration, likely through IGF-1 signaling.
The neonatal myeloid hypoxia response promotes cardiac regeneration in mice, likely mediated by IGF-1 signaling, offering potential mechanistic insights for future heart failure therapies.
Background: The adult mammalian heart lacks the regenerative potential required to replenish depleted cardiomyocytes and restore cardiac function after injury. Ischemic cardiac injury contributes to heart failure, a leading cause of death worldwide. Neonatal mice possess the capacity to regenerate injured myocardium and macrophages contribute to this process. The mechanisms contributing to the regenerative crosstalk between macrophages and cardiomyocytes remain incompletely elucidated and offer potential to inform future therapeutic strategies. Methods: ) and reconstituting HIF-dependent mitogens. In parallel, we examined epigenetic and transcriptional signatures of the cardiac macrophage response and focused on intercellular crosstalk with cardiomyocytes. Results: . Parallel multiomic analysis revealed epigenetic regenerative signatures. Conclusions: in neonatal cardiac regeneration, likely through IGF-1 signaling.
Becker et al. (Tue,) conducted a other in Ischemic cardiac injury. Reconstituting HIF-dependent mitogens was evaluated on Cardiac regeneration. The neonatal myeloid hypoxia response promotes cardiac regeneration, likely through IGF-1 signaling.
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