Welcome to the Bursac Lab

The research focus of the Bursac group is on: 1) basic studies of heart and muscle biology and pathophysiology and 2) translational studies of regenerative therapies in small and large animal models of striated muscle injury and disease. Research tools employed in these studies involve human induced pluripotent stem cells, tissue engineering, and gene editing. Specifically, a variety of 2D and 3D cell culture techniques, including use of custom-designed tissue culture bioreactors, are applied to engineer and functionally mature rodent and human heart and muscle tissues. These in vitro models are utilized in conjunction with genome editing (CRISPR/Cas9) and high-throughput sequencing to dissect the roles of structural and genetic factors that contribute cardiac and skeletal muscle function, dysfunction, and regenerative response at multiple organizational levels, from subcellular, to single cell and tissue level. Incorporation of human iPSC-derived non-muscle cells (e.g. endothelial cells, immune system cells, neurons) in engineered cardiac and skeletal muscle tissues enables realistic in vitro studies of molecular and cellular mechanisms underlying tissue injury, proliferation, migration, vascularization, innervation, inflammation, fibrosis, and regeneration. Currently, our human disease-in-a-dish modeling studies are focused on Duchenne Muscular Dystrophy, Pompe disease, dyspherlinopathy, and various types of cardiomyopathies. Towards clinical translation, the Bursac lab applies rodent models of myocardial infarction and congenital heart disease as well as volumetric skeletal muscle loss and injury to test the safety and efficacy of cell, tissue-engineering, and gene (viral) therapies for cardiac and skeletal muscle repair. In preclinical, large animal (porcine and non-human primate) models of heart attack and arrhythmias, we are exploring whether transplantation of human heart tissue “patches” or expression of pro-proliferative genes and engineered ion channels can improve cardiac function and prevent heart failure and sudden cardiac death.