Endogenous lipid-derived ligands for sensory TRP ion channels and their pain modulation

@article{Bang2010EndogenousLL,
  title={Endogenous lipid-derived ligands for sensory TRP ion channels and their pain modulation},
  author={Sangsu Bang and Sungjae Yoo and Uhtaek Oh and Sun Wook Hwang},
  journal={Archives of Pharmacal Research},
  year={2010},
  volume={33},
  pages={1509-1520},
  url={https://api.semanticscholar.org/CorpusID:25294787}
}
Endogenously generated lipids that modulate the sensory TRP activities are focused on, suggesting that information on lipidergic ligands may contribute to the understanding of peripheral pain mechanism and provide an opportunity to design novel therapeutic strategies.
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47 Citations
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47 Citations

TRP channels interaction with lipids and its implications in disease.

TRP-channels as key integrators of lipid pathways in nociceptive neurons.

Lipids as central modulators of sensory TRP channels.

Transient receptor potential ion channels in primary sensory neurons as targets for novel analgesics

It is argued that nociception‐related TRP channels on primary sensory neurons provide highly valuable targets for the development of novel analgesic and that, in order to reduce possible undesirable side effects, novel analgesics should prevent the translocation from the cytoplasm to the cell membrane and the sensitization of the channels rather than blocking the channel pore or binding sites for exogenous or endogenous activators.

Transient Receptor Potential Channels and Pain

The reader is offered an overview, relevant to chronic pain diseases, of the original as well as the most recent discoveries regarding the superfamily of TRP channels.

Venom Peptide Toxins Targeting the Outer Pore Region of Transient Receptor Potential Vanilloid 1 in Pain: Implications for Analgesic Drug Development

This review will focus on the mechanisms by which venom-derived peptides interact with this portion of TRPV1 to control receptor functions and how these mechanisms can drive the development of new types of analgesics.

Terpenes and lipids of the endocannabinoid and transient-receptor-potential-channel biosignaling systems.

The pleiotropic nature of and therapeutically relevant interactions between cananbinergic and TRP-channel signaling suggest the possibility of dual-acting ligands as drugs.

Quantitative analysis of TRP channel genes in mouse organs

The expression profile of TRP channels in major tissues provides insight to their physiological functions and therefore application to new drug development, and consistency with their functions as molecular sensors for irritants and temperature changes is shown.

Quantitative analysis of TRP channel genes in mouse organs

The expression profile of TRP channels in major tissues provides insight to their physiological functions and therefore application to new drug development, and consistency with their functions as molecular sensors for irritants and temperature changes is shown.

Beyond the classic eicosanoids: Peripherally-acting oxygenated metabolites of polyunsaturated fatty acids mediate pain associated with tissue injury and inflammation.

104 References

Noxious compounds activate TRPA1 ion channels through covalent modification of cysteines

The nervous system senses peripheral damage through nociceptive neurons that transmit a pain signal. TRPA1 is a member of the Transient Receptor Potential (TRP) family of ion channels and is…

Noxious Cold Ion Channel TRPA1 Is Activated by Pungent Compounds and Bradykinin

Farnesyl Pyrophosphate Is a Novel Pain-producing Molecule via Specific Activation of TRPV3*

Farnesyl pyrophosphate (FPP), an intermediate metabolite in the mevalonate pathway, specifically activates TRPV3 among six thermoTRPs using Ca2+ imaging and electrophysiology with cultured keratinocytes and TRpV3-overexpressing cells, suggesting that FPP is the firstly identified endogenous TRP V3 activator that causes nociception.

Cutaneous nociception evoked by 15-delta PGJ2 via activation of ion channel TRPA1

It is shown that 15d-PGJ2 induces acute nociception when administered cutaneously and does so via a TRPA1-specific mechanism.

Sensitization of TRPA1 by PAR2 contributes to the sensation of inflammatory pain.

It is shown that a functional interaction of PAR2 and TRPA1 in dorsal root ganglion (DRG) neurons could contribute to the sensation of inflammatory pain.

Citral Sensing by TRANSient Receptor Potential Channels in Dorsal Root Ganglion Neurons

Citral's broad spectrum and prolonged sensory inhibition may prove more useful than capsaicin for allodynia, itch, or other types of pain involving superficial sensory nerves and skin.

Prostaglandin-Induced Activation of Nociceptive Neurons via Direct Interaction with Transient Receptor Potential A1 (TRPA1)

Consistent with the hypothesis that TRPA1 activation required reactive electrophilic moieties, A- and J-series prostaglandins, and the isoprostane 8-iso-prostaglandin A2-evoked calcium influx in hTRPA1-HEK cells with similar potency and efficacy, data suggest a novel mechanism through which reactive prostanoids may activate nociceptive neurons independent of prostaglandsin receptors.

Cox-dependent fatty acid metabolites cause pain through activation of the irritant receptor TRPA1

It is shown that cyclopentenone PGs produce pain by direct stimulation of nociceptors via TRPA1 activation, expanding the mechanism of NSAID analgesia from blockade of indirect nocceptor sensitization by classical PGs to inhibition of direct TRPA 1-dependent nocICEptor activation by cyclopENTenonePGs.

TRPA1 Mediates the Inflammatory Actions of Environmental Irritants and Proalgesic Agents

The menthol receptor TRPM8 is the principal detector of environmental cold

It is shown that cultured sensory neurons and intact sensory nerve fibres from TRPM8-deficient mice exhibit profoundly diminished responses to cold, validating the hypothesis that TRP channels are the principal sensors of thermal stimuli in the peripheral nervous system.
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