ArticleJournal of immunology (Baltimore, Md. : 1950)2019
Development of Inflammatory Hypoxia and Prevalence of Glycolytic Metabolism in Progressing Herpes Stromal Keratitis Lesions.
Article in Journal of immunology (Baltimore, Md. : 1950), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 50 citations in OpenAlex.
- Topical Glycolysis Inhibition Restores MAVS-Associated Antiviral Signaling in Herpes Simplex Keratitis.Investigative ophthalmology & visual science · 2026Article
- Hexokinase-2 as a Therapeutic Target: Alleviating Herpes Simplex Keratitis Through Metabolic Reprogramming.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Single-Cell Transcriptomics Reveals Effects of Long-Term Contact Lens Wearing on the Human Corneal Epithelium.Investigative ophthalmology & visual science · 2025Article
- Differential homing of monocytes and neutrophils in the epithelial layer of HSV-1 infected cornea regulates viral dissemination and wound healing.The ocular surface · 2025Article
- The immunobiology of corneal HSV-1 infection and herpetic stromal keratitis.Clinical microbiology reviews · 2024Review
- Aspergillus fumigatus Hypoxia Adaptation Is Critical for the Establishment of Fungal Keratitis.Investigative ophthalmology & visual science · 2024Article
- Herpes simplex keratitis: A brief clinical overview.World journal of virology · 2024Review
- Effects of hypoxia in the diabetic corneal stroma microenvironment.Experimental eye research · 2024Article
- The HIF transcription network exerts innate antiviral activity in neurons and limits brain inflammation.Cell reports · 2024Article
- SIRT2 negatively regulates the cGAS-STING pathway by deacetylating G3BP1.EMBO reports · 2023Article
- The Aspergillus fumigatus UPR is variably activated across nutrient and host environments and is critical for the establishment of corneal infection.PLoS pathogens · 2023Article
- Hyperosmolarity promotes macrophage pyroptosis by driving the glycolytic reprogramming of corneal epithelial cells in dry eye disease.Frontiers of medicine · 2023Article
- Novel characterization of CXCR4 expressing cells in uninfected and herpes simplex virus-1 infected corneas.The ocular surface · 2023Article
- Overactivation of Norepinephrine-β2-Adrenergic Receptor Axis Promotes Corneal Neovascularization.Investigative ophthalmology & visual science · 2023Article
- Perfluorodecalin-based oxygenated emulsion as a topical treatment for chemical burn to the eye.Nature communications · 2022Article
- HSV-1 0∆NLS vaccine elicits a robust B lymphocyte response and preserves vision without HSV-1 glycoprotein M or thymidine kinase recognition.Scientific reports · 2022Article
- Diphenyleneiodonium Treatment Inhibits the Development of Severe Herpes Stromal Keratitis Lesions.Journal of virology · 2022Article
- Effects of Inflammatory Response Genes on the Immune Microenvironment in Colorectal Cancer.Frontiers in genetics · 2022Article
- Therapeutic potential of topical administration of acriflavine against hypoxia-inducible factors for corneal fibrosis.Frontiers in pharmacology · 2022Article
- Hypoxia adaptation in the cornea: Current animal models and underlying mechanisms.Animal models and experimental medicine · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Chronic inflammation in tissues often causes the development of hypoxia. Herpes stromal keratitis (HSK) is a corneal chronic inflammatory condition that develops in response to recurrent HSV-1 infection. In this study, we investigated the development of hypoxia, the expression of hypoxia-associated glycolytic genes in HSV-1 infected corneas, and the outcome of blocking hypoxia-inducible factor (HIF) dimerization on the severity of HSK. Our results showed the development of hypoxia, an elevated expression of hypoxia-associated glycolytic genes, and an increased level of lactate in corneas with progressing HSK lesions. The magnitude of hypoxia correlated with the extent of neutrophils infiltrating the infected corneas, and the depletion of neutrophils reduced the development of hypoxia in infected corneas. Additionally, in progressing HSK lesions, nuclear localization of HIF-2α protein was detected in corneal epithelial cells, whereas HIF-1α protein stabilization was observed in infiltrating immune cells. Administration of acriflavine drug to HSV-1-infected mice inhibited nuclear accumulation of HIF-1α and HIF-2α protein in immune cell types and epithelial cells, respectively, in infected corneas. As a result, a decreased influx of CD4 T cells and nongranulocytic myeloid cells, but an increased influx of neutrophils, was noted in developing HSK lesions. Interestingly, acriflavine treatment given during the clinical disease period decreased neovascularization but increased the opacity in HSV-1-infected corneas. Taken together, the results of our study lay the foundation to dissect the role of inflammatory hypoxia and hypoxia-associated genes in the pathogenesis of HSK.
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