Excessive Tumor Necrosis Factor Activation After Infarction Contributes to Susceptibility of Myocardial Rupture and Left Ventricular Dysfunction
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Interleukin-10 deficiency impairs bone marrow-derived endothelial progenitor cell survival and function in ischemic myocardiumRole of adiponectin receptors in endothelin-induced cellular hypertrophy in cultured cardiomyocytes and their expression in infarcted heartModifying the mechanics of healing infarcts: Is better the enemy of good?Quercetin inhibits left ventricular hypertrophy in spontaneously hypertensive rats and inhibits angiotensin II-induced H9C2 cells hypertrophy by enhancing PPAR-γ expression and suppressing AP-1 activity.TRB3 gene silencing alleviates diabetic cardiomyopathy in a type 2 diabetic rat modelAutonomic dysfunction is associated with high mobility group box-1 levels in patients after acute myocardial infarctionRelationships of growth factors, proinflammatory cytokines, and anti-inflammatory cytokines with long-term clinical results of autologous bone marrow mononuclear cell transplantation in STEMIMyocardial knockdown of mRNA-stabilizing protein HuR attenuates post-MI inflammatory response and left ventricular dysfunction in IL-10-null mice.Mao-to Prolongs the Survival of and Reduces TNF-alpha Expression in Mice with Viral Myocarditis.Ligusticum wallichii Extract Inhibited the Expression of IL-1β after AMI in RatsStem cell factor receptor induces progenitor and natural killer cell-mediated cardiac survival and repair after myocardial infarction.Double-stranded RNA-dependent protein kinase phosphorylation of the alpha-subunit of eukaryotic translation initiation factor 2 mediates apoptosis.Tumor necrosis factor-alpha produced in cardiomyocytes mediates a predominant myocardial inflammatory response to stretch in early volume overload.Dual roles of tumor necrosis factor-alpha receptor-1 in a mouse model of hindlimb ischemia.Differential roles of cardiac and leukocyte derived macrophage migration inhibitory factor in inflammatory responses and cardiac remodelling post myocardial infarction.Nox2 and Nox4 mediate tumour necrosis factor-α-induced ventricular remodelling in miceExercise ameliorates high fat diet induced cardiac dysfunction by increasing interleukin 10.Early postmyocardial infarction survival in Murphy Roths Large mice is mediated by attenuated apoptosis and inflammation but depends on genetic backgroundDual Endothelin Receptor Blockade Abrogates Right Ventricular Remodeling and Biventricular Fibrosis in Isolated Elevated Right Ventricular AfterloadSensing the cardiac environment: exploiting cues for regenerationPhosphatase PTEN is critically involved in post-myocardial infarction remodeling through the Akt/interleukin-10 signaling pathway.Spontaneous myocarditis mimicking human disease occurs in the presence of an appropriate MHC and non-MHC background in transgenic mice.Interleukin-10 treatment attenuates pressure overload-induced hypertrophic remodeling and improves heart function via signal transducers and activators of transcription 3-dependent inhibition of nuclear factor-κBMatrix metalloproteinases in cardiovascular diseasePeriostin is essential for cardiac healing after acute myocardial infarction.Matrix metalloproteinase-28 deletion exacerbates cardiac dysfunction and rupture after myocardial infarction in mice by inhibiting M2 macrophage activation.Early cardiac changes in a rat model of prediabetes: brain natriuretic peptide overexpression seems to be the best marker.Correlation between Platelet Gelsolin and Platelet Activation Level in Acute Myocardial Infarction Rats and Intervention Effect of Effective Components of Chuanxiong Rhizome and Red Peony Root.Cathepsin-L ameliorates cardiac hypertrophy through activation of the autophagy-lysosomal dependent protein processing pathways.The immune system and cardiac repair.Transient receptor potential vanilloid gene deletion exacerbates inflammation and atypical cardiac remodeling after myocardial infarction.Tumor necrosis factor-alpha and mortality in heart failure: a community study.Blockade of NF-kappaB using IkappaB alpha dominant-negative mice ameliorates cardiac hypertrophy in myotrophin-overexpressed transgenic mice.Effects of age on plasma matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs)The effect of polymer degradation time on functional outcomes of temporary elastic patch support in ischemic cardiomyopathy.The origin of human mesenchymal stromal cells dictates their reparative properties.Receptors for tumor necrosis factor-alpha play a protective role against obesity and alter adipose tissue macrophage statusIL-10 inhibits inflammation and attenuates left ventricular remodeling after myocardial infarction via activation of STAT3 and suppression of HuR.Monocytes in heart failure: relationship to a deteriorating immune overreaction or a desperate attempt for tissue repair?Telmisartan attenuates isoproterenol-induced cardiac remodeling in rats via regulation of cardiac adiponectin expression.
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P2860
Excessive Tumor Necrosis Factor Activation After Infarction Contributes to Susceptibility of Myocardial Rupture and Left Ventricular Dysfunction
description
im November 2004 veröffentlichter wissenschaftlicher Artikel
@de
wetenschappelijk artikel
@nl
наукова стаття, опублікована в листопаді 2004
@uk
name
Excessive Tumor Necrosis Facto ...... d Left Ventricular Dysfunction
@en
Excessive Tumor Necrosis Facto ...... d Left Ventricular Dysfunction
@nl
type
label
Excessive Tumor Necrosis Facto ...... d Left Ventricular Dysfunction
@en
Excessive Tumor Necrosis Facto ...... d Left Ventricular Dysfunction
@nl
prefLabel
Excessive Tumor Necrosis Facto ...... d Left Ventricular Dysfunction
@en
Excessive Tumor Necrosis Facto ...... d Left Ventricular Dysfunction
@nl
P2093
P1433
P1476
Excessive Tumor Necrosis Facto ...... d Left Ventricular Dysfunction
@en
P2093
Fayez Dawood
Lorrie A. Kirshenbaum
Manyin Chen
Peter P. Liu
Wen-Hu Wen
P304
P356
10.1161/01.CIR.0000147233.10318.23
P407
P50
P577
2004-11-16T00:00:00Z