Cause and effect relationship between myocardial mast cell number and matrix metalloproteinase activity. - Wikidata - awgldk - TriplyDB

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

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

http://www.wikidata.org/entity/Q44068464

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Gender differences in non-ischemic myocardial remodeling: are they due to estrogen modulation of cardiac mast cells and/or membrane type 1 matrix metalloproteinase Cardiac fibroblast: the renaissance cell.Estrogen attenuates chronic volume overload induced structural and functional remodeling in male rat hearts.Time-dependent remodeling of transmural architecture underlying abnormal ventricular geometry in chronic volume overload heart failure Inhibition of matrix metalloproteinase activity prevents increases in myocardial tumor necrosis factor-alpha.Temporal evaluation of cardiac myocyte hypertrophy and hyperplasia in male rats secondary to chronic volume overload.Cardiac kallikrein-kinin system is upregulated in chronic volume overload and mediates an inflammatory induced collagen loss.Cardiac mast cells: the centrepiece in adverse myocardial remodelling.Myocardial remodeling in diabetic cardiomyopathy associated with cardiac mast cell activation.Estrogen inhibits mast cell chymase release to prevent pressure overload-induced adverse cardiac remodeling Microarray identifies extensive downregulation of noncollagen extracellular matrix and profibrotic growth factor genes in chronic isolated mitral regurgitation in the dog Tumor necrosis factor-alpha produced in cardiomyocytes mediates a predominant myocardial inflammatory response to stretch in early volume overload.Dynamic molecular and histopathological changes in the extracellular matrix and inflammation in the transition to heart failure in isolated volume overload Opposing roles of PARP-1 in MMP-9 and TIMP-2 expression and mast cell degranulation in dyslipidemic dilated cardiomyopathy.Substance P induces adverse myocardial remodelling via a mechanism involving cardiac mast cells.The emerging prominence of the cardiac mast cell as a potent mediator of adverse myocardial remodeling Substance P in heart failure: the good and the bad.Protection from adverse myocardial remodeling secondary to chronic volume overload in mast cell deficient rats Estrogenic modulation of inflammation-related genes in male rats following volume overload Isolation of functional cardiac immune cells Prevention of adverse cardiac remodeling to volume overload in female rats is the result of an estrogen-altered mast cell phenotype.Cardiac chymase: pathophysiological role and therapeutic potential of chymase inhibitors.Stem cell factor is responsible for the rapid response in mature mast cell density in the acutely stressed heart.Volume overload induces autophagic degradation of procollagen in cardiac fibroblasts.THE AUTOCRINE ROLE OF TRYPTASE IN PRESSURE OVERLOAD-INDUCED MAST CELL ACTIVATION, CHYMASE RELEASE AND CARDIAC FIBROSIS.Cardiac fibroblasts: friend or foe?Mast Cell Inhibition Attenuates Cardiac Remodeling and Diastolic Dysfunction in Middle-aged, Ovariectomized Fischer 344 × Brown Norway Rats.The immune system and cardiac repair.Mast cells and epsilonPKC: a role in cardiac remodeling in hypertension-induced heart failure.Cardiac-restricted overexpression of extracellular matrix metalloproteinase inducer causes myocardial remodeling and dysfunction in aging mice.Estrogen modulates the influence of cardiac inflammatory cells on function of cardiac fibroblasts.ETA selective receptor antagonism prevents ventricular remodeling in volume-overloaded rats.Mast cell stabilization decreases cardiomyocyte and LV function in dogs with isolated mitral regurgitation.TNF-alpha inhibition attenuates adverse myocardial remodeling in a rat model of volume overload.Increased fibroblast chymase production mediates procollagen autophagic digestion in volume overload.Temporal changes in integrin-mediated cardiomyocyte adhesion secondary to chronic cardiac volume overload in rats.The multiple mechanistic faces of a pure volume overload: implications for therapy Cardiac fibroblast physiology and pathology.Regulation of Connective Tissue Growth Factor and Cardiac Fibrosis by an SRF/MicroRNA-133a Axis Pressure overload leads to an increased accumulation and activity of mast cells in the right ventricle.

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P2860

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

http://www.wikidata.org/entity/Q44068464

description

2002 nî lūn-bûn

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2002年の論文

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2002年学术文章

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2002年学术文章

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2002年学术文章

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2002年学术文章

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2002年学术文章

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2002年學術文章

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2002年學術文章

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2002年學術文章

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name

Cause and effect relationship ...... ix metalloproteinase activity.

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Cause and effect relationship ...... ix metalloproteinase activity.

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Cause and effect relationship ...... ix metalloproteinase activity.

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Cause and effect relationship ...... ix metalloproteinase activity.

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American Journal of Physiology - Heart and Circulatory Physiology

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Cause and effect relationship ...... ix metalloproteinase activity.

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Amanda L Chancey

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Beatriz B Matsubara

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Gregory L Brower

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Joseph S Janicki

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Srihari Thanigaraj

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P2860

Immunological characterization and functional importance of human heart mast cells.

Fibrillar collagen and remodeling of dilated canine left ventricle.

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

Mast cell collagenase correlates with regression of pulmonary vascular remodeling in the rat.

Increase in cross-linking of type I and type III collagens associated with volume-overload hypertrophy.

Transmural changes in mast cell density in rat heart after infarct induction in vivo.

Morphometric analysis of collagen network and plasma perfused capillary bed in the myocardium of rats during evolution of cardiac hypertrophy.

Mast cell distribution, activation, and phenotype in atherosclerotic lesions of human carotid arteries.

Cardiac Collagen Remodeling in the Cardiomyopathic Syrian Hamster and the Effect of Losartan

Stem Cell Factor in Mast Cells and Increased Mast Cell Density in Idiopathic and Ischemic Cardiomyopathy

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