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.
- Heart failure
- Tumour necrosis factor
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine