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Updated: Jan 11, 2026

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Effect of mitochondrial dysfunction on neuropathic pain.

Yunqi Li1, Ping Wu2, Qingping Wen2

  • 1Department of Anesthesiology, The First Affiliated Hospital of Dalian Medical University, Dalian, China; Anesthesiology Department, Dalian Medical University, Dalian, China.

Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie
|November 11, 2025
PubMed
Summary

Mitochondrial dysfunction contributes to neuropathic pain through complex mechanisms. Targeting these cellular energy issues offers promising new treatments for chronic pain conditions.

Keywords:
Adenosine triphosphateMitochondrial dysfunctionNeuropathic painOxidative stressReactive oxygen species

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Pain Research

Background:

  • Neuropathic pain, a chronic condition from nervous system damage, has limited effective treatments.
  • Mitochondria, crucial for cellular energy and neuronal homeostasis, are increasingly implicated in pain.
  • The precise role and mechanisms of mitochondrial dysfunction in neuropathic pain require further elucidation.

Purpose of the Study:

  • To review current research on how mitochondrial dysfunction influences neuropathic pain.
  • To explore the underlying molecular and cellular mechanisms involved.
  • To discuss therapeutic strategies targeting mitochondrial dysfunction for neuropathic pain.

Main Methods:

  • Literature review of recent studies on neuropathic pain and mitochondrial function.
  • Analysis of key pathways: mitochondrial morphology, bioenergetics, dynamics, oxidative stress, and autophagy.
  • Synthesis of evidence linking these mechanisms to pain signaling.

Main Results:

  • Mitochondrial dysfunction contributes to neuropathic pain via morphological changes, bioenergetic deficits (e.g., reduced ATP), and impaired dynamics (e.g., fragmentation, axonal transport issues).
  • Increased oxidative stress and disrupted mitochondrial autophagy exacerbate neuronal dysfunction and abnormal pain signal transmission.
  • These cellular alterations collectively drive neuropathic pain pathogenesis.

Conclusions:

  • Mitochondrial dysfunction is a significant factor in neuropathic pain development and maintenance.
  • Understanding these mechanisms provides a basis for novel therapeutic interventions.
  • Targeting mitochondrial pathways offers a promising avenue for precise neuropathic pain treatment.