The long term research interest in our laboratory is to understand the effect of inherited mutations in p21 Ras signaling on cardiovascular development and disease. Neurofibromatosis type 1 (NF1) is the result of inactivating mutations in the NF1 tumor suppressor gene and serves as a prototypical model of accelerated p21 Ras activity. NF1 patients are at increased risk of premature and severe cardiovascular disease, including hypertension, arterial stenosis, aneurysm formation, and Moya Moya. To interrogate these pathways, we utilize mutant and lineage-restricted transgenic mice in multiple model systems to induce cardiovascular disease. We are particularly interested in identifying patient-specific therapeutic targets and biomarkers of disease.
As a clinical neonatologist, I am also interested in understanding how prematurity and/or neonatal factors contribute to cardio-metabolic disease. We are active collaborators with investigators in the Georgia Prevention Institute and lead clinical projects focused on improving utilization and outcomes in patients undergoing extracorporeal membrane oxygenation (ECMO).
JAGWIRE: Red blood cell transfusions can increase mortality rates of newborns on ECMO, study finds
