ArticleScientific reports2023
RNA-Seq-based transcriptome analysis of corneal endothelial cells derived from patients with Fuchs endothelial corneal dystrophy.
Article in Scientific reports, 2023. 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 trial behind it
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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- Tcf4 CTG Repeat Expansion Induces RNA Toxicity and MBNL-Associated Splicing Dysregulation in a Mouse Model of Fuchs Endothelial Corneal Dystrophy.Investigative ophthalmology & visual science · 2026Article
- Targeting RhoA/ROCK Signaling to Modulate Extracellular Matrix Remodeling in Corneal Endothelial Dystrophies.Investigative ophthalmology & visual science · 2026Article
- High expression of the underexplored SLC4A11 protein-coding transcript is specific to the corneal endothelium.Scientific reports · 2026Article
- TAZ (bioRxiv : the preprint server for biology · 2026Article
- Article
- Integrated Transcriptomics and Experimental Validation Reveal That Ellagic Acid Alleviates Fuchs Endothelial Corneal Dystrophy via PLAU/NF-κB Signaling.Investigative ophthalmology & visual science · 2026Article
- Early Transcriptomic and Pathologic Changes of Col8a2 Mutant Fuchs Endothelial Corneal Dystrophy.Investigative ophthalmology & visual science · 2026Article
- Transcriptome analyses of human corneal endothelial cell lines derived from patients with Fuchs endothelial corneal dystrophy.Scientific reports · 2025Article
- The PERK-p38 MAPK Axis Drives Endoplasmic Reticulum Stress-Induced Apoptosis in Fuchs Endothelial Corneal Dystrophy.Investigative ophthalmology & visual science · 2025Article
- Review
- Generation of a Mouse Model of Fuchs Endothelial Corneal Dystrophy by Knock-in of CTG Trinucleotide Repeat Expansion in the TCF4 Gene.Investigative ophthalmology & visual science · 2025Article
- A feasibility of computational drug screening for Fuchs endothelial corneal dystrophy.Scientific reports · 2025Article
- Comprehensive analysis of splicing variants in corneal endothelial cells of patients with Fuchs endothelial corneal dystrophy.Scientific reports · 2025Article
- Comprehensive identification of dysregulated extracellular matrix molecules in the corneal endothelium of patients with Fuchs endothelial corneal dystrophy.Scientific reports · 2025Article
- Heterozygous Tcf4 Deficiency Mitigates Fuchs Endothelial Corneal Dystrophy Progression in a Mouse Model.Investigative ophthalmology & visual science · 2025Article
- The TCF4 Gene Regulates Apoptosis of Corneal Endothelial Cells in Fuchs Endothelial Corneal Dystrophy.Investigative ophthalmology & visual science · 2025Article
- How "Omics" Studies Contribute to a Better Understanding of Fuchs' Endothelial Corneal Dystrophy.Current issues in molecular biology · 2025Review
- Inherited mitochondrial dysfunction triggered by OPA1 mutation impacts the sensory innervation fibre identity, functionality and regenerative potential in the cornea.Scientific reports · 2024Article
- Dysregulation of the TCF4 Isoform in Corneal Endothelial Cells of Patients With Fuchs Endothelial Corneal Dystrophy.Investigative ophthalmology & visual science · 2024Article
- Expression and Impact of Fibronectin, Tenascin-C, Osteopontin, and Type XIV Collagen in Fuchs Endothelial Corneal Dystrophy.Investigative ophthalmology & visual science · 2024Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fuchs endothelial corneal dystrophy (FECD) is the most common inherited corneal disease. Fibrillar focal excrescences called guttae and corneal edema due to corneal endothelial cell death result in progressive vision loss. Multiple genetic variants have been reported, but the pathogenesis of FECD is not fully understood. In this study, we used RNA-Seq to analyze differential gene expression in the corneal endothelium obtained from patients with FECD. Differential expression analysis of transcriptomic profiles revealed that expression of 2366 genes (1092 upregulated and 1274 downregulated genes) was significantly altered in the corneal endothelium of patients with FECD compared to healthy subjects. Gene ontology analysis demonstrated an enrichment of genes involved in extracellular matrix (ECM) organization, response to oxidative stress, and apoptotic signaling. Several pathway analyses consistently indicated the dysregulation of ECM-associated pathways. Our differential gene expression findings support the previously proposed underlying mechanisms, including oxidative stress and apoptosis of endothelial cells, as well as the phenotypic clinical FECD hallmark of ECM deposits. Further investigation focusing on differentially expressed genes related to these pathways might be beneficial for elucidating mechanisms and developing novel therapies.
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