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Proinflammatory Cytokines Mediate GPCR Dysfunction.

Maradumane L Mohan1, Neelakantan T Vasudevan, Sathyamangla V Naga Prasad

  • 1*Department of Molecular Cardiology, Lerner Research Institute, Cleveland Clinic, Cleveland, OH; and †Cardiovascular Research Institute, Case Western Reserve University, Cleveland, OH.

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Summary
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Chronic inflammation, driven by cytokines like tumor necrosis factor-alpha (TNFα), contributes to heart failure (HF). Understanding TNFα

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Area of Science:

  • Cardiovascular Science
  • Immunology
  • Molecular Biology

Background:

  • Sustained proinflammatory cytokines are detrimental in chronic conditions like metabolic syndrome, cancer, and arthritis, posing cardiovascular risks.
  • Proinflammatory cytokines, including interleukin-1, interleukin-6, and tumor necrosis factor-alpha (TNFα), are linked to heart failure (HF) pathogenesis.
  • The limited success of anti-TNFα therapy in HF highlights an incomplete understanding of cytokine roles in cardiac function.

Purpose of the Study:

  • To review the mechanistic underpinnings of TNFα in HF pathogenesis.
  • To discuss the interplay between TNFα receptor signaling and G-protein-coupled receptors, specifically β-adrenergic receptors (βARs).
  • To elucidate the role of TNFα in regulating βAR function within the context of HF.

Main Methods:

  • Literature review of existing research on TNFα, βARs, and heart failure.
  • Analysis of evidence regarding cross-talk between TNFα receptor signaling and βAR pathways.
  • Synthesis of current understanding on how TNFα influences βAR regulation in cardiac function.

Main Results:

  • Proinflammatory cytokines play a dichotomous role, being acutely beneficial but chronically detrimental.
  • TNFα signaling pathways interact with βAR signaling, which are critical for cardiac function.
  • Evidence suggests TNFα actively modulates βAR function, impacting HF development.

Conclusions:

  • A deeper understanding of TNFα's role in HF is crucial, particularly its interaction with βARs.
  • Investigating the cross-talk between TNFα and βAR signaling may reveal novel therapeutic targets for heart failure.
  • Further research into the mechanistic details of TNFα regulation of βAR function is warranted.