Myocardial extracellular matrix remodeling in transgenic mice overexpressing tumor necrosis factor alpha can be modulated by anti-tumor necrosis factor alpha therapy. - Wikidata - awgldk - TriplyDB

Myocardial extracellular matrix remodeling in transgenic mice overexpressing tumor necrosis factor alpha can be modulated by anti-tumor necrosis factor alpha therapy.

Myocardial extracellular matrix remodeling in transgenic mice overexpressing tumor necrosis factor alpha can be modulated by anti-tumor necrosis factor alpha therapy.

http://www.wikidata.org/entity/Q30479528

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Tumour necrosis factor-alpha production in fibrosing alveolitis is macrophage subset specific Cytokines as new treatment targets in chronic heart failure Myocardial dysfunction in rheumatoid arthritis: epidemiology and pathogenesis Interplay of oxidative, nitrosative/nitrative stress, inflammation, cell death and autophagy in diabetic cardiomyopathy A study of the adult zebrafish ventricular function by retrospective Doppler-gated ultrahigh-frame-rate echocardiography Tauroursodeoxycholic acid (TUDCA) attenuates pressure overload-induced cardiac remodeling by reducing endoplasmic reticulum stress.Pro/Anti-inflammatory cytokine imbalance in postischemic left ventricular remodeling Heart regeneration in adult MRL mice Urokinase plasminogen activator induces pro-fibrotic/m2 phenotype in murine cardiac macrophages Clinical importance of beta-adrenoceptor polymorphisms in cardiovascular disease.Correlation of circulating MMP-9 with white blood cell count in humans: effect of smoking.Immunological and dermatological impact of progesterone.Transplanted bone marrow cells repair heart tissue and reduce myocarditis in chronic chagasic mice.Temporal and gefitinib-sensitive regulation of cardiac cytokine expression via chronic β-adrenergic receptor stimulation.The yin/yang of innate stress responses in the heart.Sp1 Mediates a Therapeutic Role of MiR-7a/b in Angiotensin II-Induced Cardiac Fibrosis via Mechanism Involving the TGF-β and MAPKs Pathways in Cardiac Fibroblasts.Infiltration of inflammatory cells plays an important role in matrix metalloproteinase expression and activation in the heart during sepsis.TNF and congestive heart failure: therapeutic possibilities.miR-146a targets Fos expression in human cardiac cells Tumor necrosis factor-alpha, biologic agents and cardiovascular risk.The methionine 196 arginine polymorphism of the TNF receptor 2 gene (TNFRSF1B) is not associated with worse outcomes in heart failure Relaxin suppresses atrial fibrillation in aged rats by reversing fibrosis and upregulating Na+ channels.Recent advances of TNF-alpha antagonists in rheumatoid arthritis and chronic heart failure.Impaired exercise capacity and skeletal muscle function in a mouse model of pulmonary inflammation.Role of NonO-histone interaction in TNFalpha-suppressed prolyl-4-hydroxylase alpha1 How can we cure a heart "in flame"? A translational view on inflammation in heart failure.Oxidative and nitrosative stress and fibrogenic response.Macro- and micronutrient dyshomeostasis in the adverse structural remodelling of myocardium.The pathogenesis of cardiac fibrosis.IL-1 induces proinflammatory leukocyte infiltration and regulates fibroblast phenotype in the infarcted myocardium.Effect of interleukin-15 on the course of myocarditis in Coxsackievirus B3-infected BALB/c mice.Aging, exercise, and extracellular matrix in the heart Oxidative stress and left ventricular remodelling after myocardial infarction.Transplantation of skeletal myoblasts secreting an IL-1 inhibitor modulates adverse remodeling in infarcted murine myocardium Biomarkers of pathophysiology in hypertrophic cardiomyopathy: implications for clinical management and prognosis.Transforming growth factor-beta receptor antagonism attenuates myocardial fibrosis in mice with cardiac-restricted overexpression of tumor necrosis factor.Characterization of the inflammatory and fibrotic response in a mouse model of cardiac pressure overload.Genetically altered mutant mouse models of guanylyl cyclase/natriuretic peptide receptor-A exhibit the cardiac expression of proinflammatory mediators in a gene-dose-dependent manner.Morphological and molecular changes of the myocardium after left ventricular mechanical support The G-308A polymorphism of the TNF-alpha gene does not predict changes in cardiac function in response to medical therapy for idiopathic dilated cardiomyopathy.

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P2860

Myocardial extracellular matrix remodeling in transgenic mice overexpressing tumor necrosis factor alpha can be modulated by anti-tumor necrosis factor alpha therapy.

http://www.wikidata.org/entity/Q30479528

description

2000 nî lūn-bûn

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2000 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

@hyw

2000 թվականի նոյեմբերին հրատարակված գիտական հոդված

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2000年の論文

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2000年論文

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2000年論文

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2000年论文

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Myocardial extracellular matri ...... necrosis factor alpha therapy.

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Myocardial extracellular matri ...... necrosis factor alpha therapy.

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A M Feldman

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C F McTiernan

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R Draviam

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S C Watkins

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T Kadokami

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P2860

Proinflammatory cytokines regulate tissue inhibitors of metalloproteinases and disintegrin metalloproteinase in cardiac cells

Interplay of matrix metalloproteinases, tissue inhibitors of metalloproteinases and their regulators in cardiac matrix remodeling.

In vivo stimulation of connective tissue accumulation by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+ in rat experimental wounds.

Alteration of collagen phenotypes in ischemic cardiomyopathy

Prolonged and effective blockade of tumor necrosis factor activity through adenovirus-mediated gene transfer

Pathologic hypertrophy with fibrosis: the structural basis for myocardial failure.

Remodeling of human myocardial collagen in idiopathic dilated cardiomyopathy. Role of metalloproteinases and pyridinoline cross-links.

Patterns of myocardial fibrosis.

Cardiac interstitium in health and disease: the fibrillar collagen network.

Determination of hydroxyproline.

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12257708

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11070088

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extracellular matrix

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18835

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