ReviewEye and vision (London, England)2021
Genetic mutations and molecular mechanisms of Fuchs endothelial corneal dystrophy.
Review in Eye and vision (London, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Systematic review of SLC4A11, ZEB1, LOXHD1, and AGBL1 variants in the development of Fuchs' endothelial corneal dystrophy.Frontiers in medicine · 2023Pooled it
- 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
- TCF4 trinucleotide repeat expansion drives distinct proteomic signatures in Fuchs endothelial corneal dystrophy.Scientific reports · 2026Article
- Early Transcriptomic and Pathologic Changes of Col8a2 Mutant Fuchs Endothelial Corneal Dystrophy.Investigative ophthalmology & visual science · 2026Article
- Review
- Molecular Studies ofInternational journal of molecular sciences · 2025Article
- Bioinformatic Analysis of the Value of Mitophagy and Immune Responses in Corneal Endothelial Dysfunction.Current issues in molecular biology · 2025Article
- From Genes to Disease: ReassessingInternational journal of molecular sciences · 2025Article
- Antioxidant MitoQ increases viability of human corneal endothelial cells with congenital hereditary endothelial dystrophy-associatedOphthalmic genetics · 2025Article
- Fuchs endothelial corneal dystrophy: an updated review.International ophthalmology · 2024Review
- Designing collagens to shed light on the multi-scale structure-function mapping of matrix disorders.Matrix biology plus · 2024Review
- Investigation of the functional impact of CHED- and FECD4-associated SLC4A11 mutations in human corneal endothelial cells.PloS one · 2024Article
- Adipose Mesenchymal Stem Cell-Derived Exosomes Promote the Regeneration of Corneal Endothelium Through Ameliorating Senescence.Investigative ophthalmology & visual science · 2023Article
- Ability of routinely collected clinical factors to predict good visual results after primary Descemet membrane endothelial keratoplasty: a cohort study.BMC ophthalmology · 2022Article
- Clusterin, other extracellular chaperones, and eye disease.Progress in retinal and eye research · 2022Review
- Potential role of extracellular granzyme B in wet age-related macular degeneration and fuchs endothelial corneal dystrophy.Frontiers in pharmacology · 2022Review
- Growth hormone in disease and treatment (Review).Medicine internationalReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundFuchs endothelial corneal dystrophy is a hereditary disease and the most frequent cause of corneal transplantation in the worldwide. Its main clinical signs are an accelerated decrease in the number of endothelial cells, thickening of Descemet's membrane and formation of guttae in the extracellular matrix. The cornea's ability to maintain stromal dehydration is impaired, causing painful epithelial bullae and loss of vision at the point when the amount of corneal endothelial cells cannot be compensated. At present, apart from corneal transplantation, there is no other effective treatment that prevents blindness. MAIN TEXT: In this review, we first summarized the mutations of COL8A2, TCF4, TCF8, SLC4A11 and AGBL1 genes in Fuchs endothelial corneal dystrophy. The molecular mechanisms associated with Fuchs endothelial corneal dystrophy, such as endoplasmic reticulum stress and unfolded protein response pathway, oxidative stress, mitochondrial dysregulation pathway, apoptosis pathway, mitophagy, epithelial-mesenchymal transition pathway, RNA toxicity and repeat-associated non-ATG translation, and other pathogenesis, were then explored. Finally, we discussed several potential treatments related to the pathogenesis of Fuchs endothelial corneal dystrophy, which may be the focus of future research.
conclusionsThe pathogenesis of Fuchs endothelial corneal dystrophy is very complicated. Currently, corneal transplantation is an important method in the treatment of Fuchs endothelial corneal dystrophy. It is necessary to continuously explore the pathogenesis of Fuchs endothelial corneal dystrophy and establish the scientific foundations for the development of next-generation corneal therapeutics.
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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.