期刊
BASIC RESEARCH IN CARDIOLOGY
卷 99, 期 1, 页码 18-28出版社
SPRINGER HEIDELBERG
DOI: 10.1007/s00395-003-0433-8
关键词
heart failure; cytokines; tumour necrosis factor; therapy
Immune activation plays a signicant role in the development and progression of chronic heart failure (CHF). Indeed, pro-inammatory 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 iniximab, 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 sufcient.
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