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Related Experiment Video

Updated: Jul 4, 2026

A Mouse Model for Corneal Neovascularization by Alkali Burn
04:17

A Mouse Model for Corneal Neovascularization by Alkali Burn

Published on: June 30, 2023

Experimental corneal alkali burn models: Methodological standards, biological outcomes, and translational gaps.

Pelin Kiyat1, Melis Palamar2

  • 1Izmir Democracy University, Buca Seyfi Demirsoy Training and Research Hospital, Department of Ophthalmology, Izmir, Turkiye.

Experimental Eye Research
|July 2, 2026
PubMed
Summary

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Corneal alkali burns cause severe eye trauma by damaging stem cells. This review analyzes animal models and therapies for these burns, highlighting research gaps for better treatments.

Area of Science:

  • Ophthalmology
  • Regenerative Medicine
  • Toxicology

Background:

  • Corneal chemical burns, especially alkali-induced, are severe ocular trauma.
  • Alkali burns lead to limbal stem cell depletion and irreversible conjunctivalization.
  • Animal models are crucial for understanding injury mechanisms and testing therapies.

Purpose of the Study:

  • To synthesize methodologies for establishing corneal alkali burn models.
  • To critically examine how protocol variables influence injury severity and consistency.
  • To review preclinical therapeutic strategies and identify translational gaps.

Main Methods:

  • Review of established corneal alkali burn models in animal research.
  • Analysis of protocol variables: alkali concentration, exposure duration, disc preparation.
Keywords:
Animal modelCorneal chemical burnLimbal stem cell deficiencyOcular surface reconstruction

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Last Updated: Jul 4, 2026

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07:39

Corneal and Limbal Alkali Injury Induction Using a Punch-Trephine Technique in a Mouse Model

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  • Assessment of murine, rabbit, and rat models; evaluation of outcome measurement strategies.
  • Review of preclinical therapeutic evidence: amniotic membrane, anti-angiogenics, cell transplantation, biologics, drug delivery.

    • Main Results:

    • Methodological variations significantly impact injury severity and inter-animal consistency.
    • Pathophysiological cascade involves oxidative burst, neovascularization, fibrosis, and epithelial changes.
    • Murine, rabbit, and rat models offer distinct advantages and limitations.
    • Current preclinical studies often focus on immediate post-injury interventions and may not fully replicate human disease severity.

    Conclusions:

    • Standardization of animal models and outcome measures is critical for reliable preclinical research.
    • Addressing translational gaps, such as simulating chronic injury and improving histopathological relevance, is essential.
    • Future research should prioritize diverse therapeutic approaches and robust translational validation for corneal alkali burn treatments.