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Biochemical Markers and Alterations in Keratoconus.

Rohit Shetty¹, Sharon D'Souza¹, Pooja Khamar¹

¹Department of Cornea and Refractive Surgery, Narayana Nethralaya, Bangalore, India.

Asia-Pacific Journal of Ophthalmology (Philadelphia, Pa.)

|December 16, 2020

Summary

Keratoconus (KC) is a progressive corneal thinning disease. Understanding its biochemical mediators is key to managing progression and developing targeted treatments for better patient outcomes.

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Area of Science:

Ophthalmology
Corneal Diseases
Biochemistry

Background:

Keratoconus (KC) is a common corneal ectasia affecting younger populations, characterized by progressive thinning and steepening.
Its pathogenesis involves dysregulated extracellular matrix remodeling, but initiating factors remain unclear.
KC is multifactorial, influenced by genetics, environment, oxidative stress, and eye rubbing.

Purpose of the Study:

To investigate biochemical alterations in Keratoconus.
To identify key mediators contributing to KC pathogenesis and progression.
To explore potential therapeutic targets for improved disease management.

Main Methods:

Analysis of corneal tissues (epithelium, stroma), corneal fibroblasts/keratocytes, tear fluid, aqueous humor, and blood from KC patients.
Assessment of various biochemical factors including extracellular matrix components, cellular regulators, inflammatory factors, hormones, metabolites, and chemical elements.

Main Results:

Significant alterations in multiple biochemical factors were observed in KC subjects.
These biochemical changes are implicated in disrupting extracellular matrix remodeling dynamics (collagen deposition, degradation, cross-linking).

Conclusions:

Biochemical mediator alterations are central to Keratoconus pathogenesis.
Identifying these key mediators can aid in disease monitoring, progression prediction, and targeted therapeutic development.