ArticleNature communications2018
STING-dependent sensing of self-DNA drives silica-induced lung inflammation.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 149 papers, 1 of them a synthesis that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
149 citing papers in PubMed, 1 synthesis or guideline pooled it, 279 citations in OpenAlex.
- Results from omic approaches in rat or mouse models exposed to inhaled crystalline silica: a systematic review.Particle and fibre toxicology · 2024Pooled it
- Extracellular RNA clearance by non-canonical cell-surface MDA5 protects against lung fibrosis.EMBO molecular medicine · 2026Article
- Silica Nanoparticles Elicit Pulmonary Inflammation via STING-Dependent Activation of NF-κB p65 Signaling Pathway.Biomolecules · 2026Article
- Silica Aggravates Steroid Hyporesponsiveness via STING Activation in House Dust Mite Lung Inflammation.Allergy · 2026Article
- Deciphering Pathogenesis of Silica Nanoparticle-Induced Airway Remodeling and Fibrosis: Insights from a Human Patient Cohort and a Murine Model.Nanomaterials (Basel, Switzerland) · 2026Article
- Murine models of pulmonary fibrosis: mechanisms, limitations and translational insights.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Interstitial lung disease and the STING pathway.The Journal of clinical investigation · 2026Review
- Immunological mechanisms and therapeutic approaches in pulmonary fibrosis.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- The human antibacterial factor APOL3 couples lysosomal damage to mitochondrial DNA efflux and type I IFN induction.Molecular cell · 2026Article
- cGAS-STING signaling in pollution-induced toxicity: mechanism and relieving medication.Apoptosis : an international journal on programmed cell death · 2026Review
- Chronic and non-canonical cGAS-STING activation: implications for health, disease, cancer, and emerging therapeutic opportunities.Apoptosis : an international journal on programmed cell death · 2026Review
- Emerging role of the immunoproteasome as a druggable target in lung inflammatory diseases.Respiratory research · 2026Review
- Interpreting the Theranostic Applications of Alumina and Silica Substrates in Cancer.Molecules (Basel, Switzerland) · 2026Review
- Plasma proteomics reveals the molecular features in rapidly progressive pneumoconiosis.Frontiers in immunology · 2026Article
- The cGAS-STING pathway in pulmonary infectious and sterile inflammation: differences, connections, and therapeutic implications.Frontiers in immunology · 2026Review
- Molecular Mechanisms of cGAS-STING Axis and Mitochondrial Dysfunction-Related Diseases in Humans: A Comprehensive Review.Current neuropharmacology · 2026Review
- Convergent death programs in chronic obstructive pulmonary disease: how pyroptotic and ferroptotic crosstalk reshapes therapeutic paradigms.Frontiers in immunology · 2026Review
- cGAS-STING signaling pathway as a therapeutic target in human diseases.Chinese medical journal · 2025Review
- NOX2-Dependent Phagocyte Signaling Mediates Silica-Induced Murine Lung Injury via Macrophage-Neutrophil Interactions.Inflammation · 2025Article
- Risk factors and mechanisms of immune checkpoint inhibitor-related pneumonitis.Human vaccines & immunotherapeutics · 2025Review
89 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
24 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Silica particles induce lung inflammation and fibrosis. Here we show that stimulator of interferon genes (STING) is essential for silica-induced lung inflammation. In mice, silica induces lung cell death and self-dsDNA release in the bronchoalveolar space that activates STING pathway. Degradation of extracellular self-dsDNA by DNase I inhibits silica-induced STING activation and the downstream type I IFN response. Patients with silicosis have increased circulating dsDNA and CXCL10 in sputum, and patients with fibrotic interstitial lung disease display STING activation and CXCL10 in the lung. In vitro, while mitochondrial dsDNA is sensed by cGAS-STING in dendritic cells, in macrophages extracellular dsDNA activates STING independent of cGAS after silica exposure. These results reveal an essential function of STING-mediated self-dsDNA sensing after silica exposure, and identify DNase I as a potential therapy for silica-induced lung inflammation.
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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.