ArticlePloS one2025
Caveolin-1 knockout improves CFA-induced inflammatory pain in adult mice through modulating the cGAS STING pathway and autophagy.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Research Progress on Regulating Neuroinflammation After Spinal Cord Injury by Targeting the cGAS-STING Pathway.Neuromolecular medicine · 2026Review
- Anti-Inflammatory Potential ofMicroorganisms · 2026Article
- Role of Caveolin-1 in Inflammation: Genetic Predisposition and Potential Implication for Multiple Sclerosis.Genes · 2026Review
- Electroacupuncture alleviates pain by activating the MD2/TLR4/NF-κB pathway in the ST36 acupoint.Frontiers in immunology · 2025Article
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Authors and funding
7 authors.
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Abstract
backgroundInflammatory pain poses a significant clinical challenge, with its underlying mechanisms not yet fully elucidated. This study investigated the role of Caveolin-1 (Cav1) in inflammatory pain and elucidated its molecular mechanisms.
methodsWe analyzed public databases and employed a mouse model of inflammatory pain induced by complete Freund's adjuvant (CFA). Cav1-knockout (Cav1-/-) mice were used to evaluate Cav1's function. The study incorporated behavioral tests, immunohistochemistry and molecular analyses. BV2 microglial cells served as the in vitro model.
resultsFollowing CFA injection, Cav1 expression was markedly elevated in the dorsal horn of spinal cord, correlating with pain behavior and inflammatory responses. Cav1-/- mice demonstrated significantly reduced pain behavior and inflammatory responses after CFA induction. Mechanistically, Cav1 enhanced inflammation by activating the cGAS-STING pathway and inhibiting autophagy. In BV2 microglia, Cav1 overexpression increased proinflammatory cytokine expression (TNF-α, IL-1β, IL-6) while inhibiting autophagy, whereas Cav1 knockdown produced opposing effects.
conclusionThis study reveals a novel role of Cav1 in inflammatory pain, demonstrating its regulation of inflammation through modulation of the cGAS-STING pathway and autophagy. These findings advance our understanding of the pathogenesis of inflammatory pain and identify Cav1 as a potential therapeutic target.
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