Abstract
Preterm birth and systemic hypoxia are leading complications of gestational diabetes mellitus (GDM) and are known to impede the regulatory and developmental pathways in the neonatal heart. Stressors resultant from systemic hypoxia drive aberrant cardiomyocyte proliferation, programming the heart to fail in early life. Using a rodent model of neonatal hypoxia, in combination with rat primary ventricular neonatal cardiomyocytes (PVNC’s) and H9c2 cells, we sought to determine if misoprostol, a prostaglandin E1 analogue, can prevent cardiomyocyte proliferation and what the key molecular players may be in this pathway.
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