ArticleExperimental eye research2026
Single cell RNA-seq characterization of non-fibrotic stromal wound repopulation in the rabbit.
Article in Experimental eye research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- Keratocyte Gene Expression Shaped by ECM Dimensionality: Evidence for Enhanced Quiescence in 3D Culture.Bioengineering (Basel, Switzerland) · 2026Article
- Corneal Nerves Promote Alkali Burn Repair by Modulating Macrophages and Neutrophils via Calcitonin Gene-Related Peptide.Investigative ophthalmology & visual science · 2026Article
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Authors and funding
4 authors.
Funding
Abstract
Following injury or surgery, quiescent stromal keratocytes can transition into fibroblasts or myofibroblasts leading to either transient or protracted corneal haze. In this study, we investigate the transcriptional changes associated with non-fibrotic wound healing using a transcorneal freeze injury (FI) in the rabbit, which induces full-thickness stromal cell loss without inducing keratocyte-myofibroblast transformation. In control corneas, scRNA-seq revealed multiple clusters expressing markers associated with keratocyte identity (e.g. KERA, LUM, DCN, and ALDH1A1), suggesting heterogeneity in stromal keratocytes in the uninjured stroma. On day 7 after FI, in vivo imaging revealed elongated cells with increased backscatter, consistent with fibroblast migration into the wounded region. Using scRNA-seq, two additional clusters expressing fibroblast markers were also identified. These clusters retained many markers consistent with keratocyte identity, and trajectory analysis demonstrated a continuous progression from quiescent keratocytes to fibroblasts. Both fibroblast clusters had elevated expression genes encoding tenascin C (TNC), claudin 5 (CLDN5), developmental proteoglycans (e.g., BGN, ASPN, VCAN), and cytoskeletal genes (MYL9, MYH10, CDH11), but did not express markers of myofibroblast transformation. Together these genes suggest a mechanically active but non-fibrotic phenotype. One of the two fibroblast clusters also expressed genes related to cell proliferation. By day 28, fibroblastic gene expression was reduced, consistent with resolution of wound healing. These findings define the transcriptional dynamics of intrastromal cell migration following FI and reveal a transient fibroblastic state that supports wound repopulation without fibrosis. Understanding this non-fibrotic repair mechanism could inform strategies to prevent scarring following corneal surgery or injury.
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