Tumour necrosis factor-α and the failing heart: Pathophysiology and therapeutic implications

Stephan Von Haehling, Ewa A. Jankowska, Stefan D. Anker

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)18-28
Number of pages11
JournalBasic Research in Cardiology
Issue number1
Publication statusPublished - Jan 2004


  • Cytokines
  • Heart failure
  • Therapy
  • Tumour necrosis factor

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine


Dive into the research topics of 'Tumour necrosis factor-α and the failing heart: Pathophysiology and therapeutic implications'. Together they form a unique fingerprint.

Cite this