Fuchs' Endothelial Dystrophy

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  Subject Areas on Research

  • A clinicopathologic series of primary graft failure after Descemet's stripping and automated endothelial keratoplasty. 
  • Activation of mitophagy leads to decline in Mfn2 and loss of mitochondrial mass in Fuchs endothelial corneal dystrophy. 
  • Age-severity relationships in families linked to FCD2 with retroillumination photography. 
  • Beta ig-h3 is synthesized by corneal epithelium and perhaps endotheliumin Fuchs' dystrophic corneas. 
  • Calcareous degeneration of host-donor interface after descemet membrane stripping with automated endothelial keratoplasty. 
  • Clinical course and origin of epithelium in cases of epithelial downgrowth after Descemet stripping automated endothelial keratoplasty. 
  • Clinical study of Fuchs corneal endothelial dystrophy leading to penetrating keratoplasty: a 30-year experience. 
  • Cost-effectiveness of Descemet's stripping endothelial keratoplasty versus penetrating keratoplasty. 
  • Descemet Membrane Endothelial Keratoplasty After Failed Descemet Stripping Without Endothelial Keratoplasty. 
  • Descemet Membrane Endothelial Keratoplasty: Safety and Outcomes: A Report by the American Academy of Ophthalmology. 
  • Descemet-stripping automated endothelial keratoplasty with a donor tissue injector. 
  • Effect of cornea donor graft thickness on the outcome of Descemet stripping automated endothelial keratoplasty surgery. 
  • Expansion of CTG18.1 Trinucleotide Repeat in TCF4 Is a Potent Driver of Fuchs' Corneal Dystrophy. 
  • Genetic screen of African Americans with Fuchs endothelial corneal dystrophy. 
  • Genome-wide association study identifies three novel loci in Fuchs endothelial corneal dystrophy. 
  • Genome-wide linkage scan in fuchs endothelial corneal dystrophy. 
  • Influence of Lens Status on Outcomes of Descemet Membrane Endothelial Keratoplasty. 
  • Linkage of a mild late-onset phenotype of Fuchs corneal dystrophy to a novel locus at 5q33.1-q35.2. 
  • Missense mutations in TCF8 cause late-onset Fuchs corneal dystrophy and interact with FCD4 on chromosome 9p. 
  • Missense mutations in the sodium borate cotransporter SLC4A11 cause late-onset Fuchs corneal dystrophy. 
  • Mitochondrial polymorphism A10398G and Haplogroup I are associated with Fuchs' endothelial corneal dystrophy. 
  • Mutational spectrum of the ZEB1 gene in corneal dystrophies supports a genotype-phenotype correlation. 
  • Mutations in AGBL1 cause dominant late-onset Fuchs corneal dystrophy and alter protein-protein interaction with TCF4. 
  • Mutations in LOXHD1, a recessive-deafness locus, cause dominant late-onset Fuchs corneal dystrophy. 
  • Prevalence and severity of fuchs corneal dystrophy in Tangier Island. 
  • Progression of Fuchs corneal dystrophy in a family linked to the FCD1 locus. 
  • Proteomics of Fuchs' endothelial corneal dystrophy support that the extracellular matrix of Descemet's membrane is disordered. 
  • Refractive change after descemet stripping automated endothelial keratoplasty surgery and its correlation with graft thickness and diameter. 
  • Refractive changes after descemet stripping endothelial keratoplasty: a simplified mathematical model. 
  • Replication of TCF4 through association and linkage studies in late-onset Fuchs endothelial corneal dystrophy. 
  • Replication of the TCF4 intronic variant in late-onset Fuchs corneal dystrophy and evidence of independence from the FCD2 locus. 
  • Treatment of Fuchs Endothelial Dystrophy by Descemet Stripping Without Endothelial Keratoplasty. 
  • Use of ultra-high-resolution optical coherence tomography to detect in vivo characteristics of Descemet's membrane in Fuchs' dystrophy.