Scott P. Levick

The relationship between myocardial extracellular matrix remodeling and ventricular function.

Arachidonic acid metabolism as a potential mediator of cardiac fibrosis associated with inflammation.

Inhibition of matrix metalloproteinase activity by ACE inhibitors prevents left ventricular remodeling in a rat model of heart failure.

Response of cardiac mast cells to atrial natriuretic peptide.

Protection from adverse myocardial remodeling secondary to chronic volume overload in mast cell deficient rats.

Regulation of matrix metalloproteinases is at the heart of myocardial remodeling.

Cardiac mast cells mediate left ventricular fibrosis in the hypertensive rat heart.

TNF-alpha inhibition attenuates adverse myocardial remodeling in a rat model of volume overload.

Sympathetic nervous system modulation of inflammation and remodeling in the hypertensive heart.

Inhibition of matrix metalloproteinase activity prevents increases in myocardial tumor necrosis factor-alpha.

Interleukin 6 mediates myocardial fibrosis, concentric hypertrophy, and diastolic dysfunction in rats.

Cardiac mast cells: the centrepiece in adverse myocardial remodelling.

Cardiovascular changes during maturation and ageing in male and female spontaneously hypertensive rats.

Tryptase/Protease-activated receptor 2 interactions induce selective mitogen-activated protein kinase signaling and collagen synthesis by cardiac fibroblasts.

Substance P induces adverse myocardial remodelling via a mechanism involving cardiac mast cells.

Prevention of adverse cardiac remodeling to volume overload in female rats is the result of an estrogen-altered mast cell phenotype.

The convergence of ancient chinese medicine with modern therapeutics to prevent cardiac fibrosis.

Estrogenic modulation of inflammation-related genes in male rats following volume overload.