ArticleJournal of proteome research2014
Proteomics of Fuchs' endothelial corneal dystrophy support that the extracellular matrix of Descemet's membrane is disordered.
Article in Journal of proteome research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 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.
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Who cites it
28 citing papers in PubMed, 47 citations in OpenAlex.
- Targeting RhoA/ROCK Signaling to Modulate Extracellular Matrix Remodeling in Corneal Endothelial Dystrophies.Investigative ophthalmology & visual science · 2026Article
- NAMPT Deficiency Promotes Endothelial-Mesenchymal Transition by Inhibiting Energy Metabolism and Lysosomal Acidification in Late-Onset Fuchs Endothelial Corneal Dystrophy.Investigative ophthalmology & visual science · 2026Article
- p16-mediated G0/G1 cell cycle arrest leads to SASP and fibrosis in Fuchs endothelial corneal dystrophy.Cell death & disease · 2026Article
- ATF4 regulates mitochondrial dysfunction and mitophagy, contributing to corneal endothelial apoptosis.Scientific reports · 2026Article
- Layer-Specific Proteomic Profiling of the Human Cornea Reveals Insights Into Structure and Biological Function.Investigative ophthalmology & visual science · 2026Article
- Transcriptome analyses of human corneal endothelial cell lines derived from patients with Fuchs endothelial corneal dystrophy.Scientific reports · 2025Article
- Permanent Senescence Via p16 Leads to Guttae Formation in an In Vitro Human Corneal Endothelial Cell Model.Investigative ophthalmology & visual science · 2025Article
- Identification of LRRC46 as a novel candidate gene for high myopia.Science China. Life sciences · 2024Article
- Mice Deficient in TAZ (Wwtr1) Demonstrate Clinical Features of Late-Onset Fuchs' Endothelial Corneal Dystrophy.Investigative ophthalmology & visual science · 2023Article
- The soil and the seed: The relationship between Descemet's membrane and the corneal endothelium.Experimental eye research · 2023Review
- Potential role of extracellular granzyme B in wet age-related macular degeneration and fuchs endothelial corneal dystrophy.Frontiers in pharmacology · 2022Review
- Review
- Diseases of the corneal endothelium.Experimental eye research · 2021Review
- Fuchs endothelial corneal dystrophy: The vicious cycle of Fuchs pathogenesis.Progress in retinal and eye research · 2021Review
- Prospective Application of Activity-Based Proteomic Profiling in Vision Research-Potential Unique Insights into Ocular Protease Biology and Pathology.International journal of molecular sciences · 2019Review
- The serine protease HtrA1 cleaves misfolded transforming growth factor β-induced protein (TGFBIp) and induces amyloid formation.The Journal of biological chemistry · 2019Article
- Sortilin gates neurotensin and BDNF signaling to control peripheral neuropathic pain.Science advances · 2019Article
- Conservation of the Amyloid Interactome Across Diverse Fibrillar Structures.Scientific reports · 2019Article
- Association of the Gutta-Induced Microenvironment With Corneal Endothelial Cell Behavior and Demise in Fuchs Endothelial Corneal Dystrophy.JAMA ophthalmology · 2018Article
- Extracellular Matrix and Integrin Expression Profiles in Fuchs Endothelial Corneal Dystrophy Cells and Tissue Model.Tissue engineering. Part A · 2018Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
Fuchs' endothelial corneal dystrophy (FECD) is a major corneal disorder affecting the innermost part of the cornea, leading to visual impairment. As the morphological changes in FECD are mainly observed in the extracellular matrix of the Descemet's membrane/endothelial layer, we determined the protein profiles of diseased and control tissues using two relative quantitation MS methods. The first quantitation method, based on the areas of the extracted ion chromatograms, quantified the 51 and 48 most abundant proteins of the Descemet's membrane/endothelial layer in patient and control tissues, respectively, of which 10 were significantly regulated. The results indicated that the level of type VIII collagen was unaltered even though the protein previously has been shown to be implicated in familial early-onset forms of the disease. Using the second relative quantitation method, iTRAQ, we identified 22 differentially regulated proteins, many of which are extracellular proteins known to be involved in proper assembly of the basement membrane in other tissues. In total, 26 differentially regulated proteins were identified, of which 6 proteins were regulated in both methods. These results support that the morphological changes observed in FECD are caused in part by an aberrant assembly of the extracellular matrix within the Descemet's membrane/endothelial layer.
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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.