About: Excessive Tumor Necrosis Factor Activation After Infarction Contributes to Susceptibility of Myocardial Rupture and Left Ventricular Dysfunction

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article by Mei Sun et al published 16 November 2004 in Circulation

Attributes	Values
rdf:type	Item
description	wetenschappelijk artikel (nl) article scientifique publié en 2004 (fr) наукова стаття, опублікована в листопаді 2004 (uk) im November 2004 veröffentlichter wissenschaftlicher Artikel (de) article by Mei Sun et al published 16 November 2004 in Circulation (en)
publication date	wds:Q58047222-D0E916E4-B295-4125-A810-68D4554FA867
publication date	2004-11-16 00:00:00Z (xsd:dateTime)
language of work or name	wds:Q58047222-0EEEB8AF-56E9-459A-9368-5EBD34FB1436
language of work or name	English
author name string	wds:Q58047222-1DB85FB3-4161-42BA-B192-333482257EA9 wds:Q58047222-7956A43F-F8D3-4542-86F9-B1E3A3E3CA7D wds:Q58047222-B5853269-B5E5-4757-9BA6-4CE8CC0D983D wds:Q58047222-C1628C8B-38FB-4DA1-A80A-F980871A48AB wds:Q58047222-C65208A8-91C0-4367-B9B6-05FAC5C7F62C wds:Q58047222-E5681C05-EC64-479D-82E8-764875ECDA8C
author name string	Mei Sun Manyin Chen Fayez Dawood Peter P. Liu Lorrie A. Kirshenbaum Wen-Hu Wen
rdfs:label	Excessive Tumor Necrosis Factor Activation After Infarction Contributes to Susceptibility of Myocardial Rupture and Left Ventricular Dysfunction (en) Excessive Tumor Necrosis Factor Activation After Infarction Contributes to Susceptibility of Myocardial Rupture and Left Ventricular Dysfunction (nl)
skos:prefLabel	Excessive Tumor Necrosis Factor Activation After Infarction Contributes to Susceptibility of Myocardial Rupture and Left Ventricular Dysfunction (en) Excessive Tumor Necrosis Factor Activation After Infarction Contributes to Susceptibility of Myocardial Rupture and Left Ventricular Dysfunction (nl)
name	Excessive Tumor Necrosis Factor Activation After Infarction Contributes to Susceptibility of Myocardial Rupture and Left Ventricular Dysfunction (en) Excessive Tumor Necrosis Factor Activation After Infarction Contributes to Susceptibility of Myocardial Rupture and Left Ventricular Dysfunction (nl)
author	wds:Q58047222-614698F6-6A5A-406E-A65B-B6F7C46BCFEE
author	Ian Dixon
title	wds:Q58047222-812106C5-6262-494E-9167-979677B5B88F
title	Excessive Tumor Necrosis Factor Activation After Infarction Contributes to Susceptibility of Myocardial Rupture and Left Ventricular Dysfunction (en)
page(s)	wds:Q58047222-365B8143-A8F9-439D-A68B-EB993D872156
page(s)	3221-3228
instance of	wds:Q58047222-93A5C012-FDFD-4375-8B02-6AA8C7D5E96E
instance of	scholarly article
main subject	wds:Q58047222-5BE09F98-E35D-4059-8B5A-DF970916F105 wds:Q58047222-6EA1DA9D-4D55-4ED7-9678-823C694A3518
main subject	ventricular dysfunction left ventricular dysfunction
PubMed ID	wds:Q58047222-21A2AABE-F5B9-44CF-A59B-99F3F79F5680
PubMed ID	http://rdf.ncbi.nlm.nih.gov/pubchem/reference/15533863
PubMed ID	15533863
published in	wds:Q58047222-1277204E-200A-44CC-8E06-AD97C610B909
published in	Circulation
issue	wds:Q58047222-BFB4B8C3-6C72-4197-922B-D1ACD862F8EC
volume	wds:Q58047222-236F81EC-DFD0-4ECC-975A-771F9C79BB35
issue	20
volume	110
DOI	wds:Q58047222-3061F66A-9CBB-4CE1-92AF-5F9AF31D986C
DOI	http://dx.doi.org/10.1161/01.CIR.0000147233.10318.23
DOI	10.1161/01.CIR.0000147233.10318.23
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q58047222
is cites work of	The immune system and cardiac repair. Targeted cardiac overexpression of A20 improves left ventricular performance and reduces compensatory hypertrophy after myocardial infarction IL-10 inhibits inflammation and attenuates left ventricular remodeling after myocardial infarction via activation of STAT3 and suppression of HuR. The origin of human mesenchymal stromal cells dictates their reparative properties. Cathepsin-L ameliorates cardiac hypertrophy through activation of the autophagy-lysosomal dependent protein processing pathways Regulation of collagen synthesis by inhibitory Smad7 in cardiac myofibroblasts Double-stranded RNA-dependent protein kinase phosphorylation of the alpha-subunit of eukaryotic translation initiation factor 2 mediates apoptosis Receptors for tumor necrosis factor-alpha play a protective role against obesity and alter adipose tissue macrophage status Divergent tumor necrosis factor receptor-related remodeling responses in heart failure: role of nuclear factor-kappaB and inflammatory activation Neutral sphingomyelinase inhibition participates to the benefits of N-acetylcysteine treatment in post-myocardial infarction failing heart rats Improvement in cardiac function after bone marrow cell thearpy is associated with an increase in myocardial inflammation. Tumor necrosis factor-alpha and mortality in heart failure: a community study Matrix metalloproteinase-28 deletion exacerbates cardiac dysfunction and rupture after myocardial infarction in mice by inhibiting M2 macrophage activation Modifying the mechanics of healing infarcts: Is better the enemy of good? Periostin is essential for cardiac healing after acute myocardial infarction TNFα in myocardial ischemia/reperfusion, remodeling and heart failure Cardiovascular actions of the ghrelin gene-derived peptides and growth hormone-releasing hormone. Matrix metalloproteinases in cardiovascular disease Distinctive effects of carvedilol in the non-infarct zone: remodelling of the ligated rat heart linked to oxidative stress Blockade of NF-kappaB using IkappaB alpha dominant-negative mice ameliorates cardiac hypertrophy in myotrophin-overexpressed transgenic mice Induction of tumor necrosis-alpha, p38 and JNK in the spinal cord following acute heart injury in the rat model. Contributions of cardiomyocyte-cardiac fibroblast-immune cell interactions in heart failure development Phosphatase PTEN is critically involved in post-myocardial infarction remodeling through the Akt/interleukin-10 signaling pathway Inhibiting matrix metalloproteinase by cell-based timp-3 gene transfer effectively treats acute and chronic ischemic cardiomyopathy. Stem cell factor receptor induces progenitor and natural killer cell-mediated cardiac survival and repair after myocardial infarction. Transient receptor potential vanilloid gene deletion exacerbates inflammation and atypical cardiac remodeling after myocardial infarction Role of high-mobility group box 1 protein in post-infarction healing process and left ventricular remodelling Spontaneous myocarditis mimicking human disease occurs in the presence of an appropriate MHC and non-MHC background in transgenic mice. 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 Cathepsin-L contributes to cardiac repair and remodelling post-infarction. MicroRNAs in cardiac apoptosis TRB3 gene silencing alleviates diabetic cardiomyopathy in a type 2 diabetic rat model Effects of age on plasma matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs) Human umbilical cord blood progenitor cells are attracted to infarcted myocardium and significantly reduce myocardial infarction size. Exercise ameliorates high fat diet induced cardiac dysfunction by increasing interleukin 10. Changes of collagen metabolism predict the left ventricular remodeling after myocardial infarction Pro-inflammatory cytokines mediate GPCR dysfunction Direct injection of kit ligand-2 lentivirus improves cardiac repair and rescues mice post-myocardial infarction Role of adiponectin receptors in endothelin-induced cellular hypertrophy in cultured cardiomyocytes and their expression in infarcted heart TNF-alpha modulates the migratory response of mesenchymal stem cells to TRAIL. Sensing the cardiac environment: exploiting cues for regeneration Autonomic dysfunction is associated with high mobility group box-1 levels in patients after acute myocardial infarction Monocytes in heart failure: relationship to a deteriorating immune overreaction or a desperate attempt for tissue repair? Interleukin-10 deficiency impairs bone marrow-derived endothelial progenitor cell survival and function in ischemic myocardium Myocardial knockdown of mRNA-stabilizing protein HuR attenuates post-MI inflammatory response and left ventricular dysfunction in IL-10-null mice. Tumor necrosis factor-alpha produced in cardiomyocytes mediates a predominant myocardial inflammatory response to stretch in early volume overload Cardiac intercellular communication: are myocytes and fibroblasts fair-weather friends?

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