ArticlePloS one2018
Pathological molecular mechanism of symptomatic late-onset Fuchs endothelial corneal dystrophy by bioinformatic analysis.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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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.
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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- Identification of potential therapeutic targetiScience · 2026Article
- Differential expression of transcription factors in moderate and severe Fuchs endothelial corneal dystrophy.Indian journal of ophthalmology · 2026Article
- Early Transcriptomic and Pathologic Changes of Col8a2 Mutant Fuchs Endothelial Corneal Dystrophy.Investigative ophthalmology & visual science · 2026Article
- Integrated Transcriptomics and Experimental Validation Reveal That Ellagic Acid Alleviates Fuchs Endothelial Corneal Dystrophy via PLAU/NF-κB Signaling.Investigative ophthalmology & visual science · 2026Article
- Characterisation of the role played by ELMO1, GPR141 and the intergenic polymorphism rs918980 in Fuchs' dystrophy in the Indian population.FEBS open bio · 2025Article
- How "Omics" Studies Contribute to a Better Understanding of Fuchs' Endothelial Corneal Dystrophy.Current issues in molecular biology · 2025Review
- Correlation between early corneal edema and endothelial cell loss after phacoemulsification cataract surgery.Frontiers in medicine · 2025Article
- Senescent characteristics of human corneal endothelial cells upon ultraviolet-A exposure.Aging · 2024Article
- Expression and Impact of Fibronectin, Tenascin-C, Osteopontin, and Type XIV Collagen in Fuchs Endothelial Corneal Dystrophy.Investigative ophthalmology & visual science · 2024Article
- Article
- Fuchs endothelial corneal dystrophy: an updated review.International ophthalmology · 2024Review
- Oxidative Stress and Cellular Protein Accumulation Are Present in Keratoconus, Macular Corneal Dystrophy, and Fuchs Endothelial Corneal Dystrophy.Journal of clinical medicine · 2023Article
- Cell derived matrices from bovine corneal endothelial cells as a model to study cellular dysfunction.Experimental eye research · 2023Article
- Article
- Beneficial Effects of Polydeoxyribonucleotide (PDRN) in an In Vitro Model of Fuchs Endothelial Corneal Dystrophy.Pharmaceuticals (Basel, Switzerland) · 2022Article
- Therapeutic contact lens for Fuchs endothelial corneal dystrophy: Monitoring with Scheimpflug tomography.American journal of ophthalmology case reports · 2022Article
- Incorporating Differential Gene Expression Analysis with Predictive Biomarkers to Identify Novel Therapeutic Drugs for Fuchs Endothelial Corneal Dystrophy.Journal of ophthalmology · 2021Article
- Fuchs endothelial corneal dystrophy: The vicious cycle of Fuchs pathogenesis.Progress in retinal and eye research · 2021Review
- Analyzing pre-symptomatic tissue to gain insights into the molecular and mechanistic origins of late-onset degenerative trinucleotide repeat disease.Nucleic acids research · 2020Article
- Molecular Mechanisms of Fuchs and Congenital Hereditary Endothelial Corneal Dystrophies.Reviews of physiology, biochemistry and pharmacology · 2020Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fuchs endothelial corneal dystrophy (FECD) is a degenerative disease characterized by corneal endothelial decompensation. FECD causes corneal stromal and epithelial edema and progressively develops into bullous keratopathy, which can eventually lead to blindness. However, the exact pathogenesis is unknown. In this study, we performed an in-depth bioinformatic analysis of the dataset GSE74123 to determine the differentially expressed genes (DEGs) of symptomatic late-onset FECD compared with a normal control. Gene ontology (GO) terms and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways analysis were used to analyze the pathological molecular mechanism of FECD. We found that cell senescence, reactive oxygen species (ROS), the extracellular matrix (ECM), epithelial-mesenchymal transition (EMT) and immune response-related genes play an important role in the pathological development of symptomatic late-onset FECD. In addition, we revealed that down-regulated IL-6, enhanced NF-κB activity and a suite of orchestrated chemokine responses induce fibrocyte differentiation from monocyte to dendritic cell maturation. PI3K plays a key role in the molecular mechanism of symptomatic late-onset FECD. This study enhances our understanding of the molecular mechanism of FECD pathogenesis and will improve the diagnostics and therapy of FECD patients in the future.
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