Tumour necrosis factor-α and the failing heart
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Immune activation plays a signiﬁcant role in the development and progression of chronic heart failure (CHF). Indeed, pro-inﬂammatory cytokines, especially tumour necrosis factor-α (TNFα) are activated in this condition and exert direct detrimental actions on the myocardium. Physiological dampeners of TNFα 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 TNFα have been rather disappointing. Nevertheless, TNFα antagonism remains a major target of CHF therapy, although counterbalancing this cytokine alone may not be sufﬁcient.
Key wordsHeart failure cytokines tumour necrosis factor therapy
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