Heart failure after ischemic damage remains a leading cause of death in the United States due to the inability of adult humans to regenerate their hearts after injury. In contrast, newborn mammals possess an immense capacity for complete heart regeneration. Cardiac regeneration in neonatal rodents relies on the proliferation of pre-existing heart muscle cells - called cardiomyocytes (CM) - to replace the damaged tissue. This ability is lost during the first week of development when the majority of rodent CMs undergo permanent cell cycle arrest, polyploidization, and hypertrophic growth. We’ve recently discovered that increasing levels of circulating thyroid hormones after birth drive this developmental transition. Furthermore, we identified possible interactions between thyroid hormones and adrenergic receptor signaling that further inhibit CM proliferation and cardiac regeneration. Our lab now focuses on resolving the cellular and molecular mechanisms downstream of these neurohormonal signals that restrict heart regenerative potential in mammals.
Speaker: Alexander Payumo, San Jose State University
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