Funding outcome

Immediately post birth, newborns normally undergo a major maturational increase in cardiac fatty acid oxidation (FAQ), providing a major cardiac energy substrate for ATP production. Newborns may be affected by congenital heart defects (CHDs), leading to improper heart function and the development of cardiac hypertrophy, where the heart muscle thickens and impedes blood flow. Stress from reparative surgery can cause additional hypertrophy. Post-translational modifications, such as acetylation, can regulate metabolic enzymes in cardiac FAQ, increasing FAQ, and hypertrophy delays this. My project will investigate how acetylation is mediated in the newborn heart and the impact of cardiac hypertrophy on this alteration and the mechanisms involved in newborn cardiac energy metabolism during maturation. Infant surgical heart tissue will be analyzed through lmmunoblotting and lmmunoprececipitation techniques, where the expression of acetylases, deacetylases, and FAQ enzymes in the myocardium will be measured to assess the impact of their acetylation. This research is integral to gain a better understanding of newborn cardiac energy metabolism and how changes in this can influence heart disease. Research findings will help develop novel strategies to protect newborn hearts from surgical stress and improve patient care of these newborns with CHDs.