My laboratory seeks to identify mechanisms responsible for human congenital heart disease, the most common cause of still-births in the U.S. and one of the major contributors to morbidity and mortality in infants and toddlers. We believe that by understanding the mechanisms regulating growth and differentiation of heart precursor stem/progenitor cells during early embryonic development we can then apply these principles to understand the pathogenesis heart malformation during fetal development and to leverage them for treating adult onset heart diseases such as heart failure and arrhythmia. We currently use both genetically-modified mice as our in vivo model to understand the biology of heart development as well as induced pluripotent stem cells (iPSCs) as a in vitro model to study the process of heart cell formation. Our major areas of interests include cardiovascular developmental biology, disease modeling, tissue engineering, and regenerative biology. Within each of these areas we are particularly focused on understand the major genes that regulate the proper formation of heart chambers and the consequesnces of disrupting the normal expression of these genes and how that may lead to the development of congenital heart diseases. While mouse models are useful for studying the process of heart formation, they are not exactly like the human hearts in various ways. Since human heart fetal tissue are diffulty to obtain, we have chosen to use iPSCs derived from patients with particular congenital heart diseases to study steps involved in human heart malformation. Furthermore, to bring our work closer to treating heart disease patients, we have combined our expertise in stem cell biology with 3D biopring to make engineered functional heart tissue for screening drugs and to serve as replacement tissues for damaged heart muscles.