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Updated: Jul 24, 2025

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Cellular senescence implication in mustard keratopathy.

Mohammad Soleimani1, Seyed Mahbod Baharnoori1, Kasra Cheraqpour2

  • 1Department of Ophthalmology and Visual Sciences, University of Illinois at Chicago, Chicago, IL, USA; Eye Research Center, Farabi Eye Hospital, Tehran University of Medical Sciences, Tehran, Iran.

Experimental Eye Research
|July 5, 2023
PubMed
Summary

Nitrogen mustard exposure causes cellular senescence in the cornea, leading to delayed-onset mustard keratopathy. Targeting senescence may offer new treatments for corneal damage and fibrosis.

Keywords:
AgingBeta-galactosidaseMustard gasMustard keratopathyNitrogen mustardOcular surfaceSenescence

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Area of Science:

  • Ophthalmology
  • Toxicology
  • Cellular Biology

Background:

  • Mustard agents are chemical warfare vesicants causing significant ocular surface damage.
  • Mustard keratopathy (MK) presents as corneal opacification, ulceration, and neovascularization, potentially leading to vision loss.
  • Emerging evidence suggests cellular senescence plays a role in mustard-induced injuries and impaired wound healing.

Purpose of the Study:

  • To establish the first murine model of delayed-onset mustard keratopathy (MK).
  • To investigate the role of nitrogen mustard-induced cellular senescence in the cornea.
  • To evaluate the correlation between senescence markers and corneal fibrosis.

Main Methods:

  • Developed a murine model for delayed-onset MK using nitrogen mustard.
  • Assessed pathological signs of senescence in corneal cells via beta-galactosidase staining.
  • Quantified the relationship between beta-galactosidase staining and corneal fibrosis.

Main Results:

  • Nitrogen mustard exposure induced cellular senescence in corneal cells.
  • A significant correlation was observed between beta-galactosidase staining and the degree of corneal fibrosis.
  • Senescence appears to be an underlying mechanism for chronic and late-onset ocular surface damage.

Conclusions:

  • Nitrogen mustard exposure induces corneal cell senescence, contributing to delayed-onset MK.
  • Cellular senescence is a key pathological mechanism in mustard-induced corneal injury.
  • Anti-senescence therapies hold promise for accelerating corneal healing and reducing fibrosis in MK patients.