Our lab is interested in the role that oxygen tension plays in normal and dysregulated lung development. The fetal lung develops in an environment that is hypoxic by comparison to the adult lung and this low oxygen environment is an important mediator of normal fetal lung development. As such, babies born prematurely are abruptly exposed to much higher oxygen environments, especially if they require supplemental oxygen for life support. We have focused on the role that the extracellular matrix plays in normal and aberrant lung development. Recent studies involve the role that mitochondria and the mitochondrial genome play in hyperoxia-induced lung dysmorphogenesis. We have extended these studies to a mouse model of chorioamnionitis, a condition that predisposes the fetus to premature birth, respiratory distress, and subsequent lung developmental delay.
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