ArticleSignal transduction and targeted therapy2021
Loss of FOXC1 contributes to the corneal epithelial fate switch and pathogenesis.
Article in Signal transduction and targeted therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
24 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Pooled it
- The CXXC1-IGFBP6 Axis Maintains Corneal Epithelial Differentiation via H3K4me3-Dependent Transcriptional Activation.Investigative ophthalmology & visual science · 2026Article
- Exosome-based therapies for corneal disorders: current status and future perspectives.MedScience · 2026Review
- Acute Inflammation Drives Corneal Pathological Regeneration.Investigative ophthalmology & visual science · 2026Article
- FOXC1 Regulates Cytokine Signaling, Inflammatory Pathways, and Retinoid Metabolism to Maintain Limbal Epithelial Cell Homeostasis In Vitro.International journal of molecular sciences · 2026Article
- PAX6-dependent differentiation landscape of ocular surface epithelium via single-cell RNA sequencing in hiPSC-derived ocular developmental organoid.Communications biology · 2025Article
- Glucocorticoids regulate the expression of Srsf1 through Hdac4/Foxc1 axis to induce apoptosis of osteoblasts.Communications biology · 2025Article
- miRNA Expression Profile in Primary Limbal Epithelial Cells of Aniridia Patients.Investigative ophthalmology & visual science · 2025Article
- Network analysis reveals potential mechanisms that determine the cellular identity of keratinocytes and corneal epithelial cells through the Hox/Gtl2-Dio3 miRNA axis.Frontiers in cell and developmental biology · 2025Article
- Deciphering craniopharyngioma subtypes: Single-cell analysis of tumor microenvironment and immune networks.iScience · 2024Article
- PAX6-WNK2 Axis Governs Corneal Epithelial Homeostasis.Investigative ophthalmology & visual science · 2024Article
- Deciphering the dynamic single-cell transcriptional landscape in the ocular surface ectoderm differentiation system.Life medicine · 2024Article
- Diagnostic Challenges of Axenfeld-Rieger Syndrome and a Novel FOXC1 Gene Mutation in a Polish Family.Journal of clinical medicine · 2024Article
- Congenital anterior segment ocular disorders: Genotype-phenotype correlations and emerging novel mechanisms.Progress in retinal and eye research · 2024Review
- Article
- The single-cell transcriptomic atlas and RORA-mediated 3D epigenomic remodeling in driving corneal epithelial differentiation.Nature communications · 2024Article
- Article
- Identification of the regulatory circuit governing corneal epithelial fate determination and disease.PLoS biology · 2023Article
- FoxC1 activates limbal epithelial stem cells following corneal epithelial debridement.Experimental eye research · 2023Article
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Forkhead box C1 (FOXC1) is required for neural crest and ocular development, and mutations in FOXC1 lead to inherited Axenfeld-Rieger syndrome. Here, we find that FOXC1 and paired box 6 (PAX6) are co-expressed in the human limbus and central corneal epithelium. Deficiency of FOXC1 and alternation in epithelial features occur in patients with corneal ulcers. FOXC1 governs the fate of the corneal epithelium by directly binding to lineage-specific open promoters or enhancers marked by H3K4me2. FOXC1 depletion not only activates the keratinization pathway and reprograms corneal epithelial cells into skin-like epithelial cells, but also disrupts the collagen metabolic process and interferon signaling pathways. Loss of interferon regulatory factor 1 and PAX6 induced by FOXC1 dysfunction is linked to the corneal ulcer. Collectively, our results reveal a FOXC1-mediated regulatory network responsible for corneal epithelial homeostasis and provide a potential therapeutic target for corneal ulcer.
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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.