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Journal ArticleDOI

The role of inflammatory mediators in chronic heart failure: cytokines, nitric oxide, and endothelin-1

TLDR
The main components which are thought to be relevant to the pathogenesis of CHF are cytokines, adhesion molecules, autoantibodies, nitric oxide, and endothelin-1, and this review will concentrate on these factors.
About
This article is published in International Journal of Cardiology.The article was published on 2000-01-15. It has received 177 citations till now. The article focuses on the topics: Proinflammatory cytokine.

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Citations
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Journal ArticleDOI

Oxidative stress and left ventricular remodelling after myocardial infarction

TL;DR: AsK1-deficient mice demonstrate that the ROS/ASK1 pathway is involved in necrotic as well as apoptotic cell death, indicating that ASK1 may be a therapeutic target to reduce left ventricular (LV) remodelling after MI.
Journal ArticleDOI

TNFα in atherosclerosis, myocardial ischemia/reperfusion and heart failure

TL;DR: The formation and release of TNFalpha and its downstream signal transduction cascade following activation of its two receptor subtypes is characterized, with special emphasis on the cardiovascular system.
OtherDOI

Pathophysiology of Heart Failure.

TL;DR: This summary of the pathophysiology of heart failure tries to give a compact overview of basic mechanisms and of the novel unfolding, progressive theory ofHeart failure to contribute to a more comprehensive knowledge of the disease.
Journal ArticleDOI

How to RECOVER from RENAISSANCE? The significance of the results of RECOVER, RENAISSANCE, RENEWAL and ATTACH

TL;DR: High dose anti-TNF therapy may not be useful in CHF patients, but the situation in lower doses and in patients with documented inflammatory/metabolic problems or in cardiac cachexia has not yet been adequately assessed.
Journal ArticleDOI

Do results of the ENABLE (Endothelin Antagonist Bosentan for Lowering Cardiac Events in Heart Failure) study spell the end for non-selective endothelin antagonism in heart failure?

TL;DR: The ENABLE study evaluated the effects of low dose bosentan, a non-selective endothelin receptor antagonist, in patients with severe heart failure and appeared to confer an early risk of worsening heart failure necessitating hospitalization, as a consequence of fluid retention.
References
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Journal ArticleDOI

An endotoxin-induced serum factor that causes necrosis of tumors

TL;DR: It is proposed that TNF mediates endotoxin-induced tumor necrosis, and that it may be responsible for the suppression of transformed cells by activated macrophages.
Journal ArticleDOI

Elevated Circulating Levels of Tumor Necrosis Factor in Severe Chronic Heart Failure

TL;DR: It is indicated that circulating levels of tumor necrosis factor are increased in cachectic patients with chronic heart failure and that this elevation is associated with the marked activation of the renin-angiotensin system seen in patients with end-stage cardiac disease.
Journal ArticleDOI

Decreased catecholamine sensitivity and beta-adrenergic-receptor density in failing human hearts.

TL;DR: It is concluded that in failing human hearts a decrease in beta-receptor density leads to subsensitivity of the beta-adrenergic pathway and decreased beta-agonist-stimulated muscle contraction.
Journal ArticleDOI

Effect of vasodilator therapy on mortality in chronic congestive heart failure. Results of a Veterans Administration Cooperative Study.

TL;DR: The data suggest that the addition of hydralazine and isosorbide dinitrate to the therapeutic regimen of digoxin and diuretics in patients with chronic congestive heart failure can have a favorable effect on left ventricular function and mortality.
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