ArticleFrontiers in immunology2023
Gelsevirine is a novel STING-specific inhibitor and mitigates STING-related inflammation in sepsis.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- The cGAS-STING pathway in inflammaging and neuroinflammation.Science China. Life sciences · 2026Review
- cGAS-STING signaling in aging and age-related diseases: therapeutic promise and precaution.Archives of pharmacal research · 2026Review
- Encephalopathy: Cause, Pathogenesis, and Treatment.MedComm · 2026Review
- Triphenylphosphine bromide enhances the effect of nano-micellar drug delivery system loaded with ROS inhibitor TEMPO on acute lung injury.Journal of biological engineering · 2026Article
- 4-Octyl itaconate alleviates sepsis-induced liver injury by regulating ferroptosis via the OTUB1/TRAF3 axis.Scientific reports · 2026Article
- Attenuation of cGAS-STING signaling-mediated lung inflammation during infection through autophagy induction by bioactive nanodevices.Theranostics · 2026Article
- PRRs-Dependent and Independent Mechanisms of STING Signaling in Inflammatory and Autoimmune Diseases.Biomedicines · 2025Review
- cGAS-STING signaling in brain aging and neurodegeneration: molecular links and therapeutic perspectives.Journal of neuroinflammation · 2025Review
- Targeting the cGAS-STING Pathway to Modulate Immune Inflammation in Diabetes and Cardiovascular Complications: Mechanisms and Therapeutic Insights.Current issues in molecular biology · 2025Review
- cGAS-STING targeting offers novel therapeutic regimen in sepsis-associated organ dysfunction.Cell biology and toxicology · 2025Review
- cGAS-STING targeting offers therapy choice in lung diseases.Biology direct · 2025Review
- The role of cGAS-STING pathway ubiquitination in innate immunity and multiple diseases.Frontiers in immunology · 2025Review
- Acacetin targets STING to alleviate the destabilization of the medial meniscus-induced osteoarthritis in mice.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Focus on the cGAS-STING Signaling Pathway in Sepsis and Its Inflammatory Regulatory Effects.Journal of inflammation research · 2024Review
- cGAS-STING pathway in pathogenesis and treatment of osteoarthritis and rheumatoid arthritis.Frontiers in immunology · 2024Review
- Roles of TRIM21/Ro52 in connective tissue disease-associated interstitial lung diseases.Frontiers in immunology · 2024Review
- Anti-Inflammatory Ergosteroid Derivatives from the Coral-Associated FungiMolecules (Basel, Switzerland) · 2023Article
- Mechanism and therapeutic potential of targeting cGAS-STING signaling in neurological disorders.Molecular neurodegeneration · 2023Review
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Stimulation of IFN genes (STING) is central to the production of interferon and proinflammatory cytokines in response to microbial DNA or self-DNA in the cytosol. The detrimental role of the activation of STING during sepsis has been well documented. Methods: Here, we found that gelsevirine (GS) potently inhibit interferon and inflammatory cytokine induction in macrophages exposed to STING agonists (2'3'-cGAMP, IFN stimulatory DNA (ISD), and poly(dA:dT)). I n silico docking analysis and surface plasmon resonance binding study showed that GS bonds with high affinity to the cyclic dinucleotide (CDN)-binding pocket of STING. Biotin pull-down assay also confirmed that GS competitively bonded to STING protein. Furthermore, GS inhibited 2'3'-cGAMP-induced STING dimerization and subsequent activation. In addition, GS induced K48-linked STING ubiquitination and degradation, which was likely through upregulating and recruiting TRIM21. In mice exposed to cecal ligation and puncture (CLP)-induced sepsis, post-operative administration of GS significantly extended the survival period and mitigated acute organ damage. Results: Overall, GS inhibited STING signaling by competitively binding to the CDN-binding pocket to lock STING in an inactive open conformation, while also promoting K48-linked STING ubiquitination and degradation. Conclusions: Our findings identify a novel STING-specific inhibitor that could be applied in the treatment of sepsis.
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