My lab is focused on understanding signaling and gene regulatory mechanisms that link metabolic disease to pathological cardiac remodeling and ultimately heart failure. In particular the lab is focused on delineating epigenetic mechanisms that regulate pathological cardiac hypertrophy and fibrosis under conditions of obesity and diabetes. DNA is tightly wrapped around proteins called histones to form chromatin. Post-translational modification (e.g. acetylation and methylation) of histone tails represents one epigenetic mechanism that can alter gene expression. Histone deacetylases (HDACs) and histone acetyltransferases (HATs) are one group of enzymes that can target histone tails for acetylation/deacetylation to regulate gene transcription.
Our lab uses an integrative, translational research approach that encompasses bioinformatics, in vitro cell culture, and in vivo animal models to:
- Understand how acetylation/deacetylation links metabolic disease (obesity and diabetes) to pathological cardiac remodeling and dysfunction.
- Elucidate dietary food components that act as epigenetic modifiers as well as elucidate a role for dietary epigenetic modifiers on pathological cardiac signaling, gene expression, and remodeling.
Lastly, camaraderie and teamwork are emphasized in my lab to create an exciting and productive environment geared to translate basic discoveries into potential therapies for cardio-metabolic disease.
B.S., Appalachian State University, 2003
M.S., University of North Carolina, Greensboro, 2005
Ph.D., University of North Carolina, Greensboro, 2011