Cell Reports Medicine· 2026Q1
Disruption of the Nav1.8/Ankyrin-3 interaction in nociceptors reduces pathological pain-like behaviors in mice
- 1citations
- Q1SCImago
- 2026year
Short summary
Inhibiting the interaction between Nav1.8 and Ankyrin-3 with a peptide alleviates neuropathic pain-like behaviors in mice.
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Key points
- Nav1.8/Ankyrin-3 interaction is necessary for pathological nociceptor hyperexcitability in neuroma pain.
- A short lipidated peptide (SLiP) was used to inhibit the Nav1.8/Ankyrin-3 interaction.
- Inhibition of this interaction alleviated neuropathic pain-like behaviors in mice.
- Electrophysiology, biochemistry, and proteomics were used to evaluate the interaction and peptide efficacy.
AI-generated from the title and abstract; the full text is not read.
Abstract
Treating chronic neuropathic pain is challenging due to its complex pathophysiology. Persistent changes in the somatosensory system prolong heightened states of stimulus-evoked and spontaneous pain. Nociceptor dorsal root ganglion (DRG) neurons are key contributors to neuropathic pain due to pathological plasticity following injury, leading to spontaneous ectopic and stimulus-evoked firing. Preclinical strategies to inhibit Nav1.8, a nociceptor-specific voltage-gated sodium channel, are successful in reducing neuropathic pain but have yet to produce similar results in clinical settings. Here, we evaluate the pharmacotherapeutic potential of the Nav1.8/Ank3 interaction in neuropathic pain, utilizing electrophysiology, biochemistry, and proteomic approaches. We report that Nav1.8/Ank3 interactions are necessary for maintaining pathological nociceptor hyperexcitability in neuroma pain and that inhibition of this interaction with a short lipidated peptide (SLiP) is sufficient to alleviate neuropathic pain-like behaviors in mice. This work highlights the value of reevaluating targets for pharmacological intervention to produce analgesia specific to pathological states.
The authors' abstract, as published at the source. Cell Reports Medicine, 2026 · DOI ↗
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Field: Physiology
PhysiologyMedicine