ArticleThe European respiratory journal2025
Cyclic GMP-AMP synthase expression is enhanced in systemic sclerosis-associated interstitial lung disease and stimulates inflammatory myofibroblast activation.
Article in The European respiratory journal, 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.
- Noncoding RNA TY1 reverses fibrosis in systemic sclerosis by attenuating the cGAS/STING pathway.JCI insight · 2026Article
- Centromeric α-satellite DNA is a hotspot of genotoxic damage, incomplete repair, and cytoplasmic mislocalization.bioRxiv : the preprint server for biology · 2026Article
- Type I interferon pathway activation in connective tissue disease associated interstitial lung disease.Frontiers in immunology · 2026Review
- Extracellular BAG3 is elevated in early diffuse systemic sclerosis.Military Medical Research · 2025Article
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27 authors.
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Abstract
objectiveThe lungs of patients with systemic sclerosis-associated interstitial lung disease (SSc-ILD) contain inflammatory myofibroblasts that arise in association with fibrotic stimuli and perturbed innate immunity. The cytosolic DNA-binding receptor cyclic GMP-AMP synthase (cGAS) is implicated in inflammation and fibrosis, but its involvement in SSc-ILD remains unknown. We examined cGAS expression, activity and therapeutic potential in SSc-ILD using human biospecimens, cultured fibroblasts, precision-cut lung slices and a well-accepted animal model.
methodsExpression and localisation of cGAS, cytokines and type 1 interferons were evaluated in SSc‑ILD lung tissues, bronchoalveolar lavage fluid and isolated lung fibroblasts.
resultsSSc-ILD lung tissue and bronchoalveolar lavage fluid were enriched for cGAS, cytokines and type 1 interferons. The cGAS pathway showed constitutive activation in SSc-ILD fibroblasts and was inducible in normal human lung fibroblasts by transforming growth factor-β1 or mechanical stimuli. In these settings, and in precision-cut lung slices, cGAS expression was paralleled by the production of cytokines, type 1 interferons and α-smooth muscle actin, which was mitigated by a small molecule cGAS inhibitor. These findings were recapitulated in the bleomycin mouse model.
conclusioncGAS signalling contributes to pathogenic inflammatory myofibroblast phenotypes in SSc‑ILD. Inhibiting cGAS or its downstream effectors represents a novel therapeutic approach.
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