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Updated: Jul 17, 2026

Assessment of Open Probability of the Mitochondrial Permeability Transition Pore in the Setting of Coenzyme Q Excess
07:35

Assessment of Open Probability of the Mitochondrial Permeability Transition Pore in the Setting of Coenzyme Q Excess

Published on: June 1, 2022

The Role of the Mitochondrial Permeability Transition Pore in Chronic Pain

Yuye Chen1, Xiaotong Chen1, Hu Zang1

  • 1Department of Anesthesiology and Pain Medicine, Hubei Key Laboratory of Geriatric Anesthesia and Perioperative Brain Health, and Wuhan Clinical Research Center for Geriatric Anesthesia, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

Current Neuropharmacology
|July 16, 2026
PubMed

Insights

The mitochondrial permeability transition pore (mPTP) may drive chronic pain by causing mitochondrial dysfunction. Targeting mPTP offers a potential new strategy for treating persistent pain conditions.

Area of Science:

  • Mitochondrial biology
  • Neuroscience
  • Pain research

Background:

  • The mitochondrial permeability transition pore (mPTP) is linked to cell death and oxidative stress.
  • Limited evidence suggests mPTP involvement in chronic pain development and maintenance.
  • Underlying mechanisms of mPTP in chronic pain are not fully understood.

Purpose of the Study:

  • To review current findings on mPTP in chronic pain models.
  • To discuss mPTP-mediated mitochondrial dysfunction in pain persistence.
  • To explore pharmacological strategies targeting mPTP for pain management.

Main Methods:

  • Narrative review of experimental and clinical chronic pain studies.
  • Analysis of mPTP's role in central sensitization and pain persistence.
  • Discussion of reactive oxygen species, neuroinflammation, apoptosis, and metabolic failure.

Main Results:

  • mPTP-mediated mitochondrial dysfunction may promote chronic pain.
  • Mechanisms include reactive oxygen species, neuroinflammation, apoptosis, and metabolic failure.
  • mPTP inhibitors show therapeutic potential for chronic pain.

Conclusions:

  • mPTP is a promising therapeutic target for chronic pain.
  • Further research is needed for mechanistic investigations and clinical translation.
  • This review provides a framework for studying mitochondrial mechanisms in pain.
Keywords:
Chronic paincGAS-STING pathwaymitochondrial dysfunctionmitochondrial permeability transition porereactive oxygen species

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