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Tumor Necrosis Factor-α in Heart Failure: an Updated Review

Sarah M Schumacher1, Sathyamangla V Naga Prasad2

  • 1NB50, Department of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, 9500 Euclid Avenue, Cleveland, OH, 44195, USA.

Current Cardiology Reports
|September 28, 2018
PubMed

Insights

Elevated proinflammatory cytokines like tumor necrosis factor-α (TNFα) worsen heart failure by disrupting the body's natural anti-inflammatory defenses. Understanding this cytokine-driven cardiac dysfunction is key to new therapeutic strategies.

Area of Science:

  • Cardiovascular Medicine
  • Immunology
  • Biochemistry

Background:

  • Proinflammatory cytokines, such as tumor necrosis factor-α (TNFα), are consistently elevated in patients with congestive heart failure (CHF).
  • These elevated cytokines disrupt the body's natural anti-inflammatory responses, leading to a loss of homeostasis.
  • The severity of heart failure often correlates with increased levels of TNFα and interleukin-6 (IL-6).

Purpose of the Study:

  • To review the current understanding of how TNFα potentiates heart failure.
  • To explore the mechanisms by which proinflammatory cytokines contribute to cardiac dysfunction.
  • To discuss the cross-talk between the sympathetic nervous system and proinflammatory cytokines in heart failure.

Main Methods:

  • Literature review of studies on proinflammatory cytokines in heart failure.
  • Analysis of the role of TNFα and IL-6 in cardiac dysfunction.
  • Examination of the interplay between sympathetic drive and inflammatory responses.

Main Results:

  • TNFα is a key proinflammatory cytokine that overwhelms anti-inflammatory responses in heart failure.
  • Elevated TNFα and IL-6 levels show a co-relationship with heart failure severity, suggesting biomarker potential.
  • Unchecked proinflammatory cytokines and their interaction with the sympathetic system override protective anti-inflammatory mechanisms.

Conclusions:

  • Proinflammatory cytokines, particularly TNFα, play a critical role in the pathogenesis of heart failure.
  • The cross-talk between sympathetic activation and proinflammatory cytokines significantly contributes to adverse outcomes in heart failure.
  • Further research into these mechanisms may reveal novel therapeutic targets for managing heart failure.
Abstract

Keywords:
Beta-adrenergic receptorCardiac hypertrophy and dilationG-protein coupled receptor kinasesHeart failureInterleukinsTumor necrosis factor alpha

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