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-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.
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von Haehling, S., Jankowska, E.A. & Anker, S.D. Tumour necrosis factor-α and the failing heart. Basic Res Cardiol 99, 18–28 (2004). https://doi.org/10.1007/s00395-003-0433-8
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DOI: https://doi.org/10.1007/s00395-003-0433-8