Dynamic molecular and histopathological changes in the extracellular matrix and inflammation in the transition to heart failure in isolated volume overload - Wikidata - awgldk - TriplyDB

Dynamic molecular and histopathological changes in the extracellular matrix and inflammation in the transition to heart failure in isolated volume overload

Dynamic molecular and histopathological changes in the extracellular matrix and inflammation in the transition to heart failure in isolated volume overload

http://www.wikidata.org/entity/Q35056934

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Volume overload induces differential spatiotemporal regulation of myocardial soluble guanylyl cyclase in eccentric hypertrophy and heart failure Xanthine oxidase inhibition preserves left ventricular systolic but not diastolic function in cardiac volume overload.Cardiac kallikrein-kinin system is upregulated in chronic volume overload and mediates an inflammatory induced collagen loss.Cardiomyocyte mitochondrial oxidative stress and cytoskeletal breakdown in the heart with a primary volume overload.Matricellular proteins in cardiac adaptation and disease.Temporal pattern of left ventricular structural and functional remodeling following reversal of volume overload heart failure.Genistein alleviates pressure overload-induced cardiac dysfunction and interstitial fibrosis in mice.Volume overload induces autophagic degradation of procollagen in cardiac fibroblasts.Physiologic and molecular characterization of a murine model of right ventricular volume overload.A modified approach to induce predictable congestive heart failure by volume overload in rats.Increased fibroblast chymase production mediates procollagen autophagic digestion in volume overload.Increased sarcolipin expression and adrenergic drive in humans with preserved left ventricular ejection fraction and chronic isolated mitral regurgitation.Mitochondrial protein phosphorylation as a regulatory modality: implications for mitochondrial dysfunction in heart failure.Myofilament dysfunction as an emerging mechanism of volume overload heart failure.The multiple mechanistic faces of a pure volume overload: implications for therapy Necroptotic cell death in failing heart: relevance and proposed mechanisms.Myocardial apoptosis in heart disease: does the emperor have clothes?The extracellular matrix in myocardial injury, repair, and remodeling.Anti-inflammatory effects of arbutin in lipopolysaccharide-stimulated BV2 microglial cells.Exposure to chronic alcohol accelerates development of wall stress and eccentric remodeling in rats with volume overload.Interleukin-6 signaling in patients with chronic heart failure treated with cardiac resynchronization therapy Dynamic adaptation of myocardial proteome during heart failure development Transcriptional Changes Associated with Long-Term Left Ventricle Volume Overload in Rats: Impact on Enzymes Related to Myocardial Energy Metabolism.Alterations in early filling dynamics predict the progression of compensated pressure overload hypertrophy to heart failure better than abnormalities in midwall systolic shortening.Desmin loss and mitochondrial damage precede left ventricular systolic failure in volume overload heart failure.Whole-genome profiling highlights the molecular complexity underlying eccentric cardiac hypertrophy.A Comparison of Phenomenologic Growth Laws for Myocardial Hypertrophy.Left ventricular remodelling in chronic primary mitral regurgitation: implications for medical therapy.

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Dynamic molecular and histopathological changes in the extracellular matrix and inflammation in the transition to heart failure in isolated volume overload

http://www.wikidata.org/entity/Q35056934

description

2011 nî lūn-bûn

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2011 թուականի Մարտին հրատարակուած գիտական յօդուած

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2011 թվականի մարտին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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Dynamic molecular and histopat ...... re in isolated volume overload

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Dynamic molecular and histopat ...... re in isolated volume overload

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AJPHEART.01104.2010

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American Journal of Physiology - Heart and Circulatory Physiology

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Dynamic molecular and histopat ...... re in isolated volume overload

@en

P2093

Ahsan Husain

http://www.w3.org/2001/XMLSchema#string

Betty Pat

http://www.w3.org/2001/XMLSchema#string

Chih-Chang Wei

http://www.w3.org/2001/XMLSchema#string

James D Gladden

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Junying Zheng

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Louis J Dell'italia

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Pamela Powell

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Yuan-Wen Chen

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P2860

DAVID: Database for Annotation, Visualization, and Integrated Discovery

Periostin as a novel factor responsible for ventricular dilation

Microarray identifies extensive downregulation of noncollagen extracellular matrix and profibrotic growth factor genes in chronic isolated mitral regurgitation in the dog

Sympathetic activation causes focal adhesion signaling alteration in early compensated volume overload attributable to 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.

Contemporary approach to aortic and mitral regurgitation.

Peroxisome proliferator-activated receptors and the control of fatty acid oxidation in cardiac hypertrophy.

Periostin is essential for cardiac healing after acute myocardial infarction.

LPS decreases fatty acid oxidation and nuclear hormone receptors in the kidney.

Peroxisome proliferator-activated receptors and inflammation: take it to heart.

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H2251-60

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10.1152/AJPHEART.01104.2010

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6

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300

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extracellular matrix

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3119090

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