ArticleFrontiers in immunology2020
Protective Role of the Nucleic Acid Sensor STING in Pulmonary Fibrosis.
Article in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
What it found
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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
21 citing papers in PubMed, 25 citations in OpenAlex.
- cGAS-STING signaling in aging and age-related diseases: therapeutic promise and precaution.Archives of pharmacal research · 2026Review
- Interstitial lung disease and the STING pathway.The Journal of clinical investigation · 2026Review
- Centromeric α-satellite DNA is a hotspot of genotoxic damage, incomplete repair, and cytoplasmic mislocalization.bioRxiv : the preprint server for biology · 2026Article
- The cGAS-STING Pathway in Pulmonary Diseases: Mechanisms and Therapeutic Potential.International journal of molecular sciences · 2025Review
- STING inhibition alleviates experimental peritoneal damage: potential therapeutic relevance for peritoneal dialysis.The Journal of pathology · 2025Article
- Genetic variation reveals the therapeutic potential of BRSK2 in idiopathic pulmonary fibrosis.BMC medicine · 2025Article
- Macrophage STING signaling promotes fibrosis in benign airway stenosis via an IL6-STAT3 pathway.Nature communications · 2025Article
- Advances in cGAS-STING Signaling in Fibrosis Diseases: Therapeutic Target in Pathological Scars.Journal of inflammation research · 2025Review
- Review
- Effects of Natural Products through Inhibiting Endoplasmic Reticulum Stress on Attenuation of Idiopathic Pulmonary Fibrosis.Drug design, development and therapy · 2024Review
- The role of the cGAS-STING pathway in chronic pulmonary inflammatory diseases.Frontiers in medicine · 2024Review
- Non-Interferon-Dependent Role of STING Signaling in Pulmonary Hypertension.Arteriosclerosis, thrombosis, and vascular biology · 2024Article
- Mitochondrial DNA Sensing Pathogen Recognition Receptors in Systemic Sclerosis Associated Interstitial Lung Disease: A Review.Current treatment options in rheumatology · 2023Article
- Ginseng saponin metabolite 20(S)-protopanaxadiol relieves pulmonary fibrosis by multiple-targets signaling pathways.Journal of ginseng research · 2023Article
- Beyond DNA sensing: expanding the role of cGAS/STING in immunity and diseases.Archives of pharmacal research · 2023Review
- Lung inflammation and interstitial fibrosis by targeted alveolar epithelial type I cell death.Frontiers in immunology · 2023Article
- STING Targeting in Lung Diseases.Cells · 2022Review
- A determination of pan-pathogen antimicrobials?Medicine in drug discovery · 2022Review
- Review
- The cGAS-STING pathway: more than fighting against viruses and cancer.Cell & bioscience · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Idiopathic pulmonary fibrosis (IPF) is the most common and severe type of interstitial lung disease for which current treatments display limited efficacy. IPF is largely driven by host-derived danger signals released upon recurrent local tissue damage. Here we explored the roles of self-DNA and stimulator of interferon genes (STING), a protein belonging to an intracellular DNA sensing pathway that leads to type I and/or type III interferon (IFN) production upon activation. Using a mouse model of IPF, we report that STING deficiency leads to exacerbated pulmonary fibrosis with increased collagen deposition in the lungs and excessive remodeling factors expression. We further show that STING-mediated protection does not rely on type I IFN signaling nor on IL-17A or TGF-β modulation but is associated with dysregulated neutrophils. Together, our data support an unprecedented immunoregulatory function of STING in lung fibrosis.
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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.