Join us with Alexander Payumo, PhD on Wednesday, July 27 at 5:00pm (PDT) to learn about cardiac regeneration and its potential for mammals.
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.
Alexander Payumo, PhD
Dr. Alexander Payumo pursued his PhD studies at Stanford University in the laboratory of Dr. James Chen where he characterized the role of T-box transcription factors during zebrafish embryogenesis using light-activatable chemical probes. It is during this time that he discovered his love for developmental biology. He then completed his postdoctoral studies at the Cardiovascular Research Institute at the University of California, San Francisco in the laboratory of Dr. Guo Huang where he studied mouse postnatal development as a model system to discover the physiological triggers that drive the loss of mammalian heart regenerative capacity after birth. As an Assistant Professor at San Jose State University, he now combines his passions for student mentorship, teaching, and research and investigates the molecular and cellular mechanisms downstream of hormonal signaling pathways involved in cardiomyocyte cell cycle regulation.
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