ArticleInvestigative ophthalmology & visual science2023
Znf469 Plays a Critical Role in Regulating Synthesis of ECM: A Zebrafish Model of Brittle Cornea Syndrome.
Article in Investigative ophthalmology & visual science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- ZNF469 drives TGF-β1/SMAD3-mediated extracellular matrix regulation in pulmonary fibrosis.Biomolecules & biomedicine · 2026Article
- ZNF469 promotes extracellular matrix production in normal and keloid dermal fibroblasts.Molecular medicine reports · 2025Article
- Identification of pathogenic variants in six Chinese families with keratoconus of autosomal dominant inheritance: pathogenicity analysis and variable phenotype.International ophthalmology · 2025Article
- On subcellular distribution of the zinc finger 469 protein (ZNF469) and observed discrepancy in the localization of endogenous and overexpressed ZNF469.FEBS open bio · 2025Article
- Five novelZhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2025Article
- Article
- Polymorphous corneal dystrophy subtype 3 and keratoconus aggravation after corneal refractive surgery in a three-generation family carrying bothFrontiers in genetics · 2025Article
- Brittle cornea syndrome: A novel mutation.Heliyon · 2024Article
- Review
- An Eye into the Aorta: The Role of Extracellular Matrix Regulatory GenesInternational journal of molecular sciences · 2024Review
- The transcription factor ZNF469 regulates collagen production in liver fibrosis.bioRxiv : the preprint server for biology · 2024Article
- Animal Models for the Study of Keratoconus.Cells · 2023Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Brittle cornea syndrome (BCS) is a rare autosomal recessive disorder characterized by extreme thinning and fragility of the cornea, and mutations in ZNF469 cause BCS-1. We aimed to establish a znf469 mutant zebrafish line to explore its roles and possible pathogenic mechanism in cornea development and disorder. Methods: znf4694del/4del mutant zebrafish was generated using the CRISPR/Cas9 technology. Transmission electron microscopy (TEM) was performed to examine the phenotype of the cornea in different developmental stages. RNA sequencing and quantitative real-time polymerase chain reaction were used to reveal the molecular mechanism. Results: Macroscopically, homozygous znf469 mutant zebrafish larvae exhibited a curved body from 72 hours postfertilization, similar to kyphoscoliosis, and a noninflated swimbladder at 7 days postfertilization (dpf). TEM revealed an extreme reduction of corneal stroma thickness in homozygous znf469 mutant zebrafish in both the central and peripheral cornea from the early development stage. RNA-sequencing analysis demonstrated that the znf469 mutation leads to the decreased synthesis of various extracellular matrix (ECM) components, such as collagens and proteoglycans, but increased synthesis of 26S proteasome family members. Conclusions: The results of our work indicate that znf469 is a critical gene that, as a widely considered transcription factor, may regulate the synthesis and degradation of a large number of ECM components that play an important role in corneal development.
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Registered trials
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