In addition to being the most common type of birth defect, congenital heart defects are significantly more frequent in pregnancies complicated by maternal diabetes or hyperglycemia, but the link between these conditions is yet to be uncovered. By utilizing iPSC-derived cardiomyocytes to model the conditions of hyperglycemia in vitro, I hope to draw out the mechanisms connecting the two. It is understood that reactive oxygen species are essential developmental signals at physiological levels, but also can be harmful to cells at higher concentrations, making them an attractive candidate for congenital heart defect pathogenesis. I theorize that chronic fetal exposure to elevated glucose causes oxidative stress through dysregulation of oxidative phosphorylation, which in turn disrupts metabolism and gene expression in developing cardiomyocytes.

I am participating in SuperUROP to further my science communication skills and expand on a project I am passionate about while preparing for grad school. Adjacent projects with the Boyer Lab, along with recent coursework such as 20.309 and 20.320, have prepared me well to tackle my project of understanding mechanisms of congenital heart defect pathogenesis, and I am excited to see the project develop!