ArticleKorean journal of ophthalmology : KJO2012
A novel decorin gene mutation in congenital hereditary stromal dystrophy: a Korean family.
Article in Korean journal of ophthalmology : KJO, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Genotype-Phenotype Correlations in Corneal Dystrophies: Advances in Molecular Genetics and Therapeutic Insights.Clinical & experimental ophthalmology · 2025Review
- Autosomal dominant stromal corneal dystrophy associated with a SPARCL1 missense variant.European journal of human genetics : EJHG · 2024Article
- A pediatric case of congenital stromal corneal dystrophy caused by the novel variant c.953del of the DCN gene.Human genome variation · 2023Article
- Sequence features, structure, ligand interaction, and diseases in small leucine rich repeat proteoglycans.Journal of cell communication and signaling · 2021Review
- Targeted proteomics effectively quantifies differences between native lung and detergent-decellularized lung extracellular matrices.Acta biomaterialia · 2016Article
- Regulation of corneal stroma extracellular matrix assembly.Experimental eye research · 2015Review
- Interclass small leucine-rich repeat proteoglycan interactions regulate collagen fibrillogenesis and corneal stromal assembly.Matrix biology : journal of the International Society for Matrix Biology · 2014Article
- Intracellularly-retained decorin lacking the C-terminal ear repeat causes ER stress: a cell-based etiological mechanism for congenital stromal corneal dystrophy.The American journal of pathology · 2013Article
- The regulatory roles of small leucine-rich proteoglycans in extracellular matrix assembly.The FEBS journal · 2013Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
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Abstract
A 43-year-old man developed decreased vision in the right eye that had persisted for seven years. Under slit lamp examination, corneal clouding was noted with normal endothelium and ocular structure. From the clinical evidence, we suspected that the patient had congenital hereditary stromal dystrophy (CHSD). He and his family underwent a genetic analysis. Penetrating keratoplasty was conducted, and the corneal button was investigated for histopathologic confirmation via both light and electron microscopy. The histopathologic results revealed mildly loosened stromal structures, which exhibited an almost normal arrangement and differed slightly from the previous findings of CHSD cases. With regard to the genetic aspects, the patient and his mother harbored a novel point mutation of the decorin gene. This genetic mutation is also distinct from previously described deletion mutations of the decorin gene. This case involved delayed penetration of mild clinical symptoms with the histological feature of a loosened fiber arrangement in the corneal stroma. We concluded that this condition was a mild form of CHSD. However, from another perspective, this case could be considered as "decorin gene-associated corneal dystrophy," which is distinct from CHSD. Further evaluation will be required for appropriate clinical, histopathologic and genetic approaches for such cases.
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