ArticleInternational journal of molecular sciences2020
The STING-IFN-β-Dependent Axis Is Markedly Low in Patients with Relapsing-Remitting Multiple Sclerosis.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 23 citations in OpenAlex.
- The cGAS-STING Pathway: A Double-Edged Regulator of Neuroinflammation and Myelin Regeneration.Molecular neurobiology · 2026Review
- cGAS-STING pathway modulation: A new hope for neural regeneration.Neural regeneration research · 2026Article
- cGAS-STING axis: A central regulator of neural homeostasis and neuroinflammatory pathogenesis.Neural regeneration research · 2026Article
- The Role and Mechanism of the cGAS-STING/NLRP3 Signaling Axis-Regulated p38 MAPK/NF-κB Pathway in Manganese-Induced Tau Aggregation-Mediated Neurotoxicity.Environment & health (Washington, D.C.) · 2026Article
- STING Mediates Microglial Polarization to Promote Neuroinflammation in Epilepsy-Related Cognitive Dysfunction.Neurochemical research · 2026Article
- STING Signaling Deficiency Exacerbates Demyelination and Immune Infiltration in Focal EAE Lesions.NeuroSci · 2025Article
- The STING Signaling: A Novel Target for Central Nervous System Diseases.Cellular and molecular neurobiology · 2025Review
- Microglial cGAS Deletion Preserves Intercellular Communication and Alleviates Amyloid-β-Induced Pathogenesis of Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Recent advancements in cGAS-STING activation, tumor immune evasion, and therapeutic implications.Medical oncology (Northwood, London, England) · 2024Review
- Mitophagy and cGAS-STING crosstalk in neuroinflammation.Acta pharmaceutica Sinica. B · 2024Review
- STING-Triggered CNS Inflammation in Human Neurodegenerative Diseases.Biomedicines · 2023Article
- Multiple Sclerosis: Inflammatory and Neuroglial Aspects.Current issues in molecular biology · 2023Review
- Neuroinflammation: The Pathogenic Mechanism of Neurological Disorders.International journal of molecular sciences · 2022Article
- cGAS- Stimulator of Interferon Genes Signaling in Central Nervous System Disorders.Aging and disease · 2021Review
- Crosstalk between Interleukin-1β and Type I Interferons Signaling in Autoinflammatory Diseases.Cells · 2021Review
- The Complexity of the cGAS-STING Pathway in CNS Pathologies.Frontiers in neuroscience · 2021Review
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cyclic GMP-AMP-synthase is a sensor of endogenous nucleic acids, which subsequently elicits a stimulator of interferon genes (STING)-dependent type I interferon (IFN) response defending us against viruses and other intracellular pathogens. This pathway can drive pathological inflammation, as documented for type I interferonopathies. In contrast, specific STING activation and subsequent IFN-β release have shown beneficial effects on experimental autoimmune encephalomyelitis (EAE) as a model for multiple sclerosis (MS). Although less severe cases of relapse-remitting MS (RRMS) are treated with IFN-β, there is little information correlating aberrant type I IFN signaling and the pathologic conditions of MS. We hypothesized that there is a link between STING activation and the endogenous production of IFN-β during neuroinflammation. Gene expression analysis in EAE mice showed that
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.