2004
DOI: 10.1161/01.res.0000130526.20854.fa
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Inflammatory Cytokines and Postmyocardial Infarction Remodeling

Abstract: Abstract-Inflammatory response and cytokine elaboration are particularly active after myocardial infarction and contribute to cardiac remodeling and eventual host outcome. The triggers of cytokine release in the acute postinfarction period include mechanical deformation, ischemic stimulus, reactive oxygen species (ROS), and cytokine selfamplification pathways. Acutely, the elaboration of tumor necrosis factor, IL-1 and IL-6, transforming growth factor families of cytokines, contribute to survival or deaths of … Show more

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Cited by 937 publications
(724 citation statements)
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References 114 publications
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“…This cardiac inflammation is linked with decreased LV function, not only in diabetic cardiomyopathy, but also for example in myocardial infarction, pressure overload, and dilated cardiomyopathy [20][21][22]. Increased cytokines are one of the mechanisms leading to LV dysfunction in diabetes mellitus, as demonstrated by an inverse correlation between dP/dt max and TNF-α in diabetic animals in this study.…”
Section: Cardiac Inflammationsupporting
confidence: 58%
See 1 more Smart Citation
“…This cardiac inflammation is linked with decreased LV function, not only in diabetic cardiomyopathy, but also for example in myocardial infarction, pressure overload, and dilated cardiomyopathy [20][21][22]. Increased cytokines are one of the mechanisms leading to LV dysfunction in diabetes mellitus, as demonstrated by an inverse correlation between dP/dt max and TNF-α in diabetic animals in this study.…”
Section: Cardiac Inflammationsupporting
confidence: 58%
“…Cytokines attenuate myocyte contractility, achieving this directly through the reduction of systolic cytosolic calcium via alterations in sarcoplasmic reticulum function and indirectly by down-regulating sarcoplasmic calcium ATPase expression, as reviewed [22]. Inflammatory cytokines were originally thought to be produced only by circulating lymphocytes, but recent evidence suggests a direct role of cardiomyocytes in pro-inflammatory cytokine production [23,24].…”
Section: Cardiac Inflammationmentioning
confidence: 99%
“…Numerous studies have demonstrated activation of cytokine cascades in the infarcted myocardium [142], [143], [144]. Induction and release of the pro-inflammatory cytokines TNF-α, IL-1β and IL-6 is consistently found in experimental models of myocardial infarction [144], [145], [11].…”
Section: Pro-inflammatory Cytokines In Myocardial Infarctionmentioning
confidence: 99%
“…However, the possible deficiency in total glutathione in the failing heart, and its related possible metabolic consequences have been overlooked. TNF-α is not expressed in the normal heart but is upregulated in the failing heart [7,22,23]. TNF-α exerts its main biological functions in its soluble form (sTNF-α), binding to the membrane TNF-R1 receptor that mediates multiple distinct pathways [24], including oxidative stress and neutral sphingomyelinase (N-SMase) activation.…”
Section: Introductionmentioning
confidence: 99%