Repair of Corneal Epithelial Defects.

Abstract

The corneal epithelium, a stratified squamous non-keratinized layer of 50-60 μm thickness, forms the outermost barrier of the cornea and provides both optical clarity and protection against trauma, infection, and fluid imbalance. It plays a vital role in protecting the eye and maintaining visual clarity. A range of conditions, including trauma, metabolic disorders, microbial infection, and limbal stem cell deficiency, can lead to chronic corneal epithelial defects and subsequent visual impairment. Epithelial renewal is a continuous process, primarily sustained by stem cells located at the limbus. These stem cells give rise to transient amplifying cells, which migrate centripetally and superficially to maintain epithelial integrity. Wound healing follows a highly regulated sequence, superficial cells slide to cover the defect, basal cells proliferate, and corneal nerves realign to support epithelial stratification. This process is orchestrated by cytoskeletal remodeling, integrin-matrix interactions, and growth factor signaling. The epithelium relies on glucose from the corneal stroma, primarily metabolized through glycolysis, while mitochondrial oxidative phosphorylation generates the ATP required for repair. Thus, epithelial regeneration is closely tied to cellular energy availability. Enhancing this process involves supporting mitochondrial function, metabolic signaling pathways, and stem cell activity. Emerging strategies in regenerative ophthalmology include NAD⁺ replenishment, activation of AMP-activated protein kinase (AMPK), application of growth factors, targeted nanotherapies, and photobiomodulation. This chapter explores these cutting-edge approaches aimed at promoting energy-driven regeneration of the corneal surface.