ArticleInvestigative ophthalmology & visual science2024
Mitochondrial DNA-Activated cGAS-STING Signaling in Environmental Dry Eye.
Article in Investigative ophthalmology & visual science, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Impact of tumor immunotherapy on kidney injury and multi-organ outcomes: a mechanistic and clinical perspective.Frontiers in immunology · 2026Pooled it
- A dual-responsive CO-releasing nanogel ameliorates retinal ischemia-reperfusion injury by restoring mitochondrial homeostasis and attenuating cGAS-STING pathway activation.Materials today. Bio · 2026Article
- The cGAS-STING pathway in senescence and aging-related diseases: mechanisms and therapeutic opportunities.Cell communication and signaling : CCS · 2026Review
- Remodeling of Metabolic and Secretory Organelles During Oncogenic and Oncomodulatory Viral Infections.Viruses · 2026Review
- Exploiting the role of milk extracellular vesicles: a comprehensive analysis on isolation methods, characterization, surface modifications, and their therapeutic applications.Journal of nanobiotechnology · 2026Review
- Protective effects of human umbilical cord mesenchymal stem cells-derived small extracelluar vesicles on corneal epithelial cells under hyperosmotic stress: Inhibition of oxidative damage and inflammation.Genetics and molecular biology · 2026Article
- Fenofibrate in ophthalmology: therapeutic efficacy and mechanisms.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2026Review
- Therapeutic Approaches Involving Mitochondria in the Treatment of Acute Kidney Injury.Seminars in nephrology · 2026Review
- STING agonism in brain tumours: mechanisms, challenges, and therapeutic advances.Frontiers in oncology · 2026Review
- cGAS-STING signaling pathway as a therapeutic target in human diseases.Chinese medical journal · 2025Review
- Cyclosporine A Ameliorates Inflammatory Responses in Dry Eye by Inactivating cGAS-STING Signaling Via the Initiation of Autophagy.Investigative ophthalmology & visual science · 2025Article
- Dry Eye Disease and Psychiatric Disorders: Neuroimmune Mechanisms and Therapeutic Perspectives.International journal of molecular sciences · 2025Review
- cGAS-STING pathway-mediated inflammatory response and its role in corneal fibrosis mechanisms.Molecular biology reports · 2025Review
- Cyclic GMP-AMP Synthase (cGAS) Deletion Promotes Less Prominent Inflammatory Macrophages and Sepsis Severity in Catheter-Induced Infection and LPS Injection Models.International journal of molecular sciences · 2025Article
- Mitochondrial DNA release via the mitochondrial permeability transition pore activates the cGAS-STING pathway, exacerbating inflammation in acute Kawasaki disease.Cell communication and signaling : CCS · 2024Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: The cGAS-STING pathway has been shown to be an important mediator of inflammation. There is emerging evidence of the importance of this signaling cascade in a variety of inflammatory diseases settings. Here, we present evidence that the mitochondrial DNA (mtDNA) damage-mediated cGAS-STING pathway plays an important role in the induction of inflammation in environmental dry eye (DE). Methods: RT-qPCR and Western blot were used to assess the induction of the cGAS-STING pathway and inflammatory cytokines in environmental DE mouse model, primary human corneal epithelial cells (pHCECs), and patients with DE. RNA sequencing was used to determine mRNA expression patterns of high osmotic pressure (HOP)-stimulated pHCECs. mtDNA was detected with electron microscopy, flow cytometry, and immunofluorescent staining. mtDNA was isolated and transfected into pHCECs for evaluating the activation of the cGAS-STING pathway. Results: The expression levels of cGAS, STING, TBK1, IRF3, and IFNβ were significantly increased in an environmental DE model and HOP-stimulated pHCECs. The STING inhibitor decreased the expression of inflammatory factors in DE. An upregulation of STING-mediated immune responses and IRF3 expression mediated by TBK1 were observed in the HOP group. HOP stimulation induced mitochondrial oxidative damage and the leakage of mtDNA into the cytoplasm. Then, mtDNA activated the cGAS-STING pathway and induced intracytoplasmic STING translocated to the Golgi apparatus. Finally, we also found activated cGAS-STING signaling in the human conjunctival blot cell of patients with DE. Conclusions: Our findings suggest that the cGAS-STING pathway is activated by recognizing cytoplasmic mtDNA leading to STING translocation, further exacerbating the development of inflammation in environmental DE.
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