We are identifying the cellular and molecular networks that governing cardiac wound healing and repair to leverage these networks as a means of developing interventions directed at enhancing repair and/or mitigating the fibrotic response.
Cellular and molecular mechanisms of cardiac wound healing and the fibrotic injury response
The impact of fibrosis and scarring on cardiac regeneration and cellular therapeutics
Signaling mechanisms govering cardiac muscle growth and remodeling
Skeletal muscle regeneration and fibrosis
The Davis lab studies how the heart heals and remodels in response to acquired and genetic diseases. Because of the heart’s limited regenerative capacity, an injury or chronic disease results in permanent fibrotic scarring, which in turn creates an environment hostile to regeneration and cellular therapies. By harnessing the power of mouse genetics, cellular engineering, genome-wide screening, and a variety of interdisciplinary experimental approaches our research is centered on elucidating the cellular and molecular underpinnings of cardiac remodeling. Specifically, this research program is focused on 3 primary areas which include (1) identifying the signaling networks causal for cardiac fibroblast differentiation into the cell-type (myofibroblast) that is causal for fibrosis and (2) manipulating the myofibroblast to improve healing after injury, and (3) identifying the mechanical signaling that determines cardiac myocyte directional growth leading to a hypertrophic or dilated heart. This research program will significantly inform the field’s understanding of fibroblast and myocyte biology as well as cardiac remodeling, which could significantly impact both drug development and the current clinical paradigms for treating acquired and genetic heart disease.
Ph.D. Molecular & Integrative Physiology, University of Michigan, Ann Arbor, 2007
M.A. Exercise & Nutritional Science, San Diego State University, 2001
B.S. Kinesiology, University of Michigan, Ann Arbor, 1996