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cGAS-STING-NFκB PATHWAY PLAYS A ROLE IN BURN INJURY-INDUCED MUSCLE WASTING.

Fei Xie, Zerong You, Bin Yan1

  • 1Department of Ophthalmology, The Second Xiangya Hospital of Central South University, Changsa, China.

Shock (Augusta, Ga.)
|May 7, 2025
PubMed
Summary

Burn injury causes muscle wasting by activating the cGAS-STING-NFκB pathway. A STING inhibitor, C176, effectively reduced muscle loss in mice by blocking this inflammatory response.

Keywords:
Burn injurycGAS-STING-NFκBinflammatory cytokinesmitochondrial DNAmuscle wasting

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Area of Science:

  • Inflammation and immunology
  • Muscle physiology
  • Burn injury research

Background:

  • Muscle wasting (MW) is a common and severe complication following burn injury (BI).
  • The cGAS-STING-NFκB signaling pathway is implicated in inflammatory responses to cellular damage.
  • This pathway's role in burn-induced muscle wasting was investigated.

Purpose of the Study:

  • To determine if the cGAS-STING-NFκB pathway contributes to muscle wasting after burn injury.
  • To evaluate the efficacy of C176, a STING inhibitor, in mitigating burn-induced muscle wasting.

Main Methods:

  • Male C57BL/6 J mice underwent sham or burn injury (30% body surface area) with or without daily C176 treatment for 14 days.
  • Muscle analysis included cytokine expression, immune cell infiltration, signaling pathway activation, and muscle proteolytic proteins (MuRF1, atrogin-1).
  • In vitro studies used C2C12 cells exposed to macrophage-derived mitochondrial DNA (mtDNA) to mimic inflammation, with or without C176.

Main Results:

  • C176 treatment significantly reduced muscle wasting in burn-injured mice (tibialis: 22%, gastrocnemius: 13%).
  • C176 inhibited the cGAS-STING-NFκB pathway, decreased inflammatory cell infiltration, and preserved neuromuscular junctions in burn-injured mice.
  • In vitro, C176 suppressed inflammatory cytokine release and muscle proteolytic protein expression induced by LPS and mtDNA.

Conclusions:

  • Activation of the cGAS-STING-NFκB pathway is a key driver of muscle wasting following burn injury.
  • C176 demonstrates therapeutic potential by effectively reducing muscle loss through inhibition of this inflammatory pathway.