My research is focused on the field of cardiovascular disease and cardiac tissue engineering. An important component of my current thesis research is to better understand the complex bidirectional cardiomyocyte-fibroblast interactions potentially involving complex bidirectional signaling through direct cell-cell contacts, paracrine actions, and/or extracellular matrix-mediated effects. I have been combining the use of diseased mouse models and tissue engineering techniques to systematically assess how disease-induced changes in fibroblast phenotype alter the electrical and mechanical function of cardiomyocyte in vitro and determine the underlying molecular mechanisms. Through this and future studies, I hope to discover novel fibroblast-related targets leading to more efficient drug or gene therapies for heart disease.
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I am studying how disease-induced changes in fibroblast phenotype alter the electrical and mechanical function of 3D engineered cardiac tissues and determine the underlying molecular mechanisms.