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Mitochondrial DAMPs produce inflammatory hyperalgesia via stimulator of interferon genes (STING) activation in DRG

Hiroaki Amino1, Ayaka Higashi1, Shunsuke Yamakita1

  • 1Department of Anesthesiology, Kyoto Prefectural University of Medicine, Kyoto, Japan.

Molecular Pain
|March 13, 2026
PubMed

Insights

Mitochondrial debris triggers inflammatory pain by activating the stimulator of interferon genes (STING) pathway in sensory neurons. Inhibiting STING reduces pain, suggesting it as a therapeutic target for inflammatory hyperalgesia.

Area of Science:

  • Neuroscience
  • Immunology
  • Pain Research

Background:

  • Damage-associated molecular patterns (DAMPs), including mitochondrial molecules, are implicated in immune responses and pain sensitization.
  • Tissue inflammation can lead to the release of mitochondrial debris, potentially contributing to pain signaling.

Purpose of the Study:

  • To investigate if mitochondrial debris promotes inflammatory hyperalgesia via STING pathway activation in dorsal root ganglion (DRG) neurons.
  • To assess the therapeutic potential of STING inhibition in pain models.

Main Methods:

  • Rats received local administration of mitochondrial debris or Complete Freund's Adjuvant (CFA) to induce inflammation and hyperalgesia.
  • Stimulator of interferon genes (STING) expression in DRG neurons was measured.
  • The effects of a selective STING inhibitor (H-151) on hyperalgesia and STING expression were evaluated.

Main Results:

  • Mitochondrial debris induced mechanical hyperalgesia and increased STING expression in DRG neurons.
  • STING inhibition with H-151 attenuated debris-induced hyperalgesia and STING upregulation.
  • In the CFA model, H-151 also alleviated inflammatory hyperalgesia and reduced STING expression.

Conclusions:

  • Mitochondrial debris activates the STING pathway in primary afferent neurons, contributing to inflammatory hyperalgesia.
  • STING activation in peripheral sensory neurons plays a pronociceptive role.
  • Targeting the STING pathway offers a potential novel therapeutic strategy for inflammatory pain.
Keywords:
DAMPMitochondriaSTINGdorsal root ganglionhyperalgesia

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