Scott Levick, PhD
Pharmacology & Toxicology
Myocardial remodeling refers to alterations in the cellular and extracellular components of the heart. Myocardial remodeling occurs as a result of adverse stimuli such as pressure overload (e.g. hypertension, aortic stenosis), volume overload (e.g. mitral regurgitation) or injury (e.g. myocardial infarction). My laboratory has two main areas of interests relating to the underlying mechanisms leading to adverse myocardial remodeling and ultimately heart failure: 1) the role of sensory nerves in mediating adverse myocardial remodeling; and 2) the mechanisms by which cardiac mast cells interact with other inflammatory cells and cardiac fibroblasts to regulate myocardial remodeling.
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McLarty JL, Melendez GC, Brower GL, Janicki JS, Levick SP. Tryptase/PAR-2 interactions induce selective MAPK signaling and collagen synthesis by cardiac fibroblasts. Hypertension, 2011;58:264-270.
Levick SP, Melendez GC, Plante E, McLarty JL, Brower GL, Janicki JS. Cardiac mast cells: the center piece in adverse myocardial remodeling. Cardiovascular Research. 2011; 89:12-19.
Levick SP, Murray DB, Janicki JS, Brower GL. Sympathetic nervous system modulation of inflammation and remodeling in the hypertensive heart. Hypertension, 2010;55:270-276.
Melendez GC, McLarty JL, Levick SP, Du Y, Janicki JS, Brower GL. Interleukin-6 Mediates Myocardial Fibrosis, Concentric Hypertrophy and Diastolic Dysfunction in Rats. Hypertension, 2010;56:225-231.