Presentation description

The goal for my 2025 research project is to test the overall hypothesis that FBXO44 degradation in cardiomyocytes results in cardiomyopathy. Our in vitro approach will consist of using Neonatal rat ventricular myocytes (NRVMs) isolated from male and female newborn rats, with gain and loss of function of FBXO44. To do so we will test the hypothesis that the degradation of FBXO44 in NRVMs will result in cardiac hypertrophy. We will measure cell size and expression of hypertrophic genes, as well as after exposing the cells to a hypertrophic stimulus. Part of our in vivo approach includes Quantitative real time PCR (qPCR) used to measure stretch markers in the heart which will help us determine whether or not the heart has experienced cardiac hypertrophy. The two genotypes we will be using include a non-Cre wild-type mice and αMHC-Cre FBXO44 knockout (KO) mice. Together, these studies will unveil the role of FBXO44 in mediating cardiac growth and will determine the sex-specific effect of FBXO44 loss and gain of function in the heart. These data are impactful because cardiomyopathy is a prominent issue in the United States and there is currently no known cure. Funding for this project was provided by the American Heart Association 25IAUST1374429.