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Oxidative-stress related increase in keratoconus tear MDA and GPX3 while NRF2-antioxidant functions decrease in

Madhuri A Koduri1, Mackenzie Charter1, Rohini Sonar2

  • 1Department of Ophthalmology, NYU Grossman School of Medicine, Science Building, Fifth Floor 435 E 30th, New York, NY, USA.

Biorxiv : the Preprint Server for Biology
|November 26, 2025
PubMed
Summary
This summary is machine-generated.

Keratoconus (KC) is linked to oxidative stress, with elevated tear Malondialdehyde (MDA) and Glutathione Peroxidase 3 (GPX3) indicating disease severity. NRF2 pathway modulation shows potential for restoring corneal health.

Keywords:
BiomarkerGPX3KeratoconusMDANRF2Oxidative stress

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Area of Science:

  • Ophthalmology
  • Molecular Biology
  • Biochemistry

Background:

  • Keratoconus (KC) is a degenerative corneal disease lacking early diagnostic biomarkers and curative treatments.
  • Understanding KC's underlying biology, particularly the role of oxidative stress, is crucial for therapeutic development.

Purpose of the Study:

  • To investigate the role of unresolved oxidative stress in keratoconus pathogenesis.
  • To identify potential biomarkers for early KC diagnosis and severity prediction.
  • To explore therapeutic strategies targeting oxidative stress pathways.

Main Methods:

  • Measured tear Malondialdehyde (MDA) and Glutathione Peroxidase 3 (GPX3) levels in KC patients and controls.
  • Correlated biomarker levels with maximal keratometry (Kmax) as a measure of KC severity.
  • Utilized a cell culture model to assess oxidative stress effects on corneal stromal cells and NRF2 pathway activity.
  • Investigated the effects of NRF2 inhibition and sulforaphane (NRF2 booster) treatment on cellular phenotype and gene expression.

Main Results:

  • Tear MDA and GPX3 were significantly elevated in KC patients and correlated positively with Kmax.
  • KC corneal stromal cells exhibited increased apoptosis and impaired NRF2 activation under oxidative stress.
  • NRF2 inhibition induced KC-like cellular phenotypes, while sulforaphane restored antioxidant gene expression and collagen deposition.

Conclusions:

  • Dysregulation of cellular antioxidant signaling is implicated in keratoconus.
  • Elevated tear MDA and GPX3 show promise as biomarkers for KC diagnosis and severity.
  • Sulforaphane treatment demonstrates potential restorative effects on KC cellular phenotypes.