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LXRs agonists alleviate fat transplantation-induced cognitive dysfunction by inhibiting STING-dependent type I
Juan Li1, Yanqiong Wu2, Fan Jiang1
1Department of Anesthesiology and Pain Medicine, Hubei Key Laboratory of Geriatric Anesthesia and Perioperative Brain Health, Wuhan Clinical Research Center for Geriatric Anesthesia, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
International Immunopharmacology
|January 20, 2026
Summary
Adipose tissue dysfunction contributes to cognitive decline in neuropathic pain via the cGAS-STING pathway. LXRβ activation can mitigate this by inhibiting the pathway, offering new therapeutic targets.
Area of Science:
- Neuroscience
- Immunology
- Metabolic disease
Background:
- Cognitive decline is frequently observed alongside neuropathic pain.
- Adipose tissue metabolism is implicated in cognitive dysfunction.
Purpose of the Study:
- To investigate the link between adipose tissue and neuropathic pain-induced cognitive dysfunction.
- To explore the role of the cGAS-STING pathway and LXRβ in this process.
Main Methods:
- Construction of an adipose tissue transplantation model in mice.
- Analysis of double-stranded DNA (dsDNA) expression, cGAS-STING pathway activation, type I interferon response, and microglial activation.
- Administration of a Liver X receptor beta (LXRβ) agonist.
Main Results:
- Adipose tissue transplantation exacerbated cognitive dysfunction.
- Increased dsDNA levels activated the cGAS-STING pathway, leading to interferon response and microglial activation.
- LXRβ agonist treatment ameliorated cognitive dysfunction by inhibiting the cGAS-STING pathway.
Conclusions:
- Adipose tissue dysfunction contributes to neuropathic pain-related cognitive decline.
- The cGAS-STING pathway and microglial activation are key mediators.
- LXRβ agonists represent a potential therapeutic strategy for cognitive dysfunction.
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