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Oxidized Lipids in Persistent Pain States.

Tabea Osthues1, Marco Sisignano2

  • 1Fraunhofer Institute for Molecular Biology and Applied Ecology IME, Branch for Translational Medicine and Pharmacology TMP, Frankfurt, Germany.

Frontiers in Pharmacology
|November 5, 2019
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Summary

Persistent and neuropathic pain, often caused by chemotherapy or nerve injuries, has limited treatment options. Signaling lipids, like oxidized linoleic acid metabolites, are key mediators in pain pathways and potential targets for new pain relief strategies.

Keywords:
HODEeicosanoidslinoleic acid metaboliteslipids inflammatory painneuropathic painpaintransient receptor potential channels

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Area of Science:

  • Neuroscience
  • Biochemistry
  • Pharmacology

Background:

  • Persistent and neuropathic pain arise from neuronal sensitization, reducing the activation threshold of sensory neurons to stimuli.
  • Current treatments are insufficient for many patients, necessitating novel therapeutic approaches.
  • Signaling lipids are critical mediators in the onset and maintenance of pain, influencing ion channel activity and neuronal signaling.

Purpose of the Study:

  • To discuss the molecular mechanisms of oxidized linoleic acid metabolites and eicosanoids in pain.
  • To evaluate these lipid mediators as potential targets for novel analgesic drug development.
  • To explore therapeutic strategies for persistent and neuropathic pain.

Main Methods:

  • Review of preclinical studies on lipid mediators and TRP channels.
  • Analysis of signaling pathways involving G-protein coupled receptors and protein kinases.
  • Critical evaluation of oxidized linoleic acid metabolites and eicosanoids in pain modulation.

Main Results:

  • Oxidized linoleic acid metabolites (HODEs, DiHOMEs, EpOMEs), eicosanoids (EETs), lysophospholipids, sphingolipids, and SPMs play distinct roles in pain transmission and inhibition.
  • Lipids can act as endogenous ligands or sensitize transient receptor potential (TRP)-channels, enhancing sensory neuron activity.
  • These mediators involve G-protein coupled receptors and intracellular protein kinases in pain signaling.

Conclusions:

  • Oxidized linoleic acid metabolites and related lipid mediators are crucial in neuropathic pain pathogenesis.
  • Targeting these lipid signaling pathways offers a promising avenue for developing new analgesics.
  • Further research into these mechanisms could lead to effective treatments for difficult-to-manage pain conditions.