Joseph S. Janicki

Effects of mast cells on the behavior of isolated heart fibroblasts: modulation of collagen remodeling and gene expression.

Effects of matrix metalloproteinase inhibition on ventricular remodeling due to volume overload.

Cardiac mast cell-mediated activation of gelatinase and alteration of ventricular diastolic function.

Gender differences in cardiac remodeling secondary to chronic volume overload.

Cause and effect relationship between myocardial mast cell number and matrix metalloproteinase activity.

The role of myocardial fibrillar collagen in ventricular remodeling and function.

Cardiac mast cell- and chymase-mediated matrix metalloproteinase activity and left ventricular remodeling in mitral regurgitation in the dog.

Gender mediated cardiac protection from adverse ventricular remodeling is abolished by ovariectomy.

The dynamic interaction between matrix metalloproteinase activity and adverse myocardial remodeling.

THE HEMODYNAMIC SPECTRUM OF ACUTE MYOCARDIAL INFARCTION: A REVIEW AND IDENTIFICATION OF THE HIGH-RISK PATIENT.

Endothelin-1 mediates cardiac mast cell degranulation, matrix metalloproteinase activation, and myocardial remodeling in rats.

Expression of matrix metalloproteinase activity in idiopathic dilated cardiomyopathy: a marker of cardiac dilatation.

Modulation of cardiac mast cell-mediated extracellular matrix degradation by estrogen.

Effects of dietary phytoestrogens on cardiac remodeling secondary to chronic volume overload in female rats.

Pharmacologic inhibition of mast cell degranulation prevents left ventricular remodeling induced by chronic volume overload in rats.

Quality assessment of graduate programs.

Cardiac mast cell regulation of matrix metalloproteinase-related ventricular remodeling in chronic pressure or volume overload.

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.

Cardioprotection in female rats subjected to chronic volume overload: synergistic interaction of estrogen and phytoestrogens.

Effects of nonselective endothelin-1 receptor antagonism on cardiac mast cell-mediated ventricular remodeling in rats.

Defective intracellular Ca2+ homeostasis contributes to myocyte dysfunction during ventricular remodelling induced by chronic volume overload in rats.

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

ETA selective receptor antagonism prevents ventricular remodeling in volume-overloaded rats.

Targeting the Nrf2 pathway against cardiovascular disease.

Nrf2 protects against maladaptive cardiac responses to hemodynamic stress.

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

Estrogen attenuates chronic volume overload induced structural and functional remodeling in male rat hearts.

Dihydro-CDDO-trifluoroethyl amide (dh404), a novel Nrf2 activator, suppresses oxidative stress in cardiomyocytes.

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.

Temporal evaluation of cardiac myocyte hypertrophy and hyperplasia in male rats secondary to chronic volume overload.

Cardiac mast cells: the centrepiece in adverse myocardial remodelling.

Up-regulation of p27(kip1) contributes to Nrf2-mediated protection against angiotensin II-induced cardiac hypertrophy.

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

Tryptase activates isolated adult cardiac fibroblasts via protease activated receptor-2 (PAR-2).

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.