title: Tumour necrosis factor-alpha and the failing heart--pathophysiology and therapeutic implications.
abstract: Immune activation plays a significant role in the development and progression of chronic heart failure (CHF). Indeed, pro-inflammatory cytokines, especially tumour necrosis factor-alpha (TNFalpha) are activated in this condition and exert direct detrimental actions on the myocardium. Physiological dampeners of TNFalpha production, such as interleukin-10, catecholamines, cortisol, and others fail in the course of the disease. However, the outcomes of two large-scale clinical trials with etanercept and infliximab, which directly antagonise TNFalpha have been rather disappointing. Nevertheless, TNFalpha antagonism remains a major target of CHF therapy, although counterbalancing this cytokine alone may not be sufficient.
authors.affiliation: Imperial College School of Medicine, National Heart & Lung Institute, Department of Clinical Cardiology, London, UK. stephan.von.haehling@web.de
authors.forename: Stephan
authors.initials: S
authors.lastname: von Haehling
authors.forename: Ewa A
authors.initials: EA
authors.lastname: Jankowska
authors.forename: Stefan D
authors.initials: SD
authors.lastname: Anker
mesh_terms: D006333:Heart Failure / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D018124:Receptors, Tumor Necrosis Factor / Q000378:metabolism; D015398:Signal Transduction; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors / Q000096:biosynthesis / Q000502:physiology*
chemical_list: D018124:Receptors, Tumor Necrosis Factor; D014409:Tumor Necrosis Factor-alpha