The role of inflammatory mediators in chronic heart failure: cytokines, nitric oxide, and endothelin-1.
There is now considerable evidence to suggest that neurohormonal and immune mechanisms may play a central role in the pathogenesis of chronic heart failure (CHF), which is likely to have important implications for the management of this condition. It has been proposed that CHF is a state of immune activation with inflammatory cytokines contributing to both the central and the peripheral manifestations of this syndrome. The immune system is the body's natural defence mechanism against infection and other stresses, which has several different components that interact with each other in a complex manner. 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. This article will also discuss the potential role of anti-cytokine therapies in the treatment of CHF.
Sharma
R
R
Cardiac Medicine, National Heart & Lung Institute, Imperial College School of Medicine, London, UK.
Coats
A J
AJ
Anker
S D
SD
D001323:Autoantibodies / Q000502:physiology; D002303:Cardiac Output, Low / Q000188:drug therapy / Q000276:immunology* / Q000503:physiopathology; D015815:Cell Adhesion Molecules / Q000502:physiology; D002908:Chronic Disease; D016207:Cytokines / Q000502:physiology*; D019332:Endothelin-1 / Q000502:physiology*; D006801:Humans; D018836:Inflammation Mediators; D009569:Nitric Oxide / Q000502:physiology*; D018384:Oxidative Stress / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology
D001323:Autoantibodies; D015815:Cell Adhesion Molecules; D016207:Cytokines; D019332:Endothelin-1; D018836:Inflammation Mediators; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide