Dr. Porter's laboratory studies mechanisms that control cardiac development, concentrating on the roles played by the intracellular organelles, mitochondria. Using in vivo and in vitro mouse models of cardiac development, the lab has shown that mitochondrial structure and function changes dramatically in cardiac myocytes as the embryonic heart forms. In particular, we have found that closure of the mitochondrial permeability transition pore (PTP) between the early and mid-embryonic period leads to a maturation of the structure of individual mitochondria and of the mitochondrial network throughout the cell. This also leads to an activation of oxidative phosphorylation, or ATP production, by mitochondria as the heart develops. These changes also cause a drop in cellular oxidative stress due to altered mitochondrial production of reactive oxygen species, and this signals to the myocytes to undergo further differentiation. More recent research finds that the same phenomena occur in the neonatal heart, and that closure of the PTP in the neonate increases cardiac function in vivo.
