The impact of hyperglycemia on the corneal epithelium: Molecular mechanisms and insight.

Type 2 Diabetes Mellitus (T2DM) is reaching epidemic levels worldwide and with it, there is a significant increase in complications associated with the disease. T2DM affects virtually all organ systems including the eye. While frequently overlooked, diabetic keratopathy is the most common ocular complication of diabetes and can manifest in mild to severe forms, the latter of which poses a major threat to vision. As the initial barrier between the environment and the eye, the corneal epithelium functions in innate immune defense. Compromise of this barrier may predispose the cornea to infection and can hinder the refractive capabilities of the eye. The clinical burden in patients with diabetic keratopathy lies primarily in the inability of the corneal epithelium to repair damage and maintain its tight barrier function. Current therapies for diabetic keratopathy are supportive, centering on the prevention of infection and promotion of an optimal healing environment. With no clear disease-modifying agent identified as of yet, a thorough understanding of the pathophysiology that underlies the development of diabetic keratopathy at the cellular level is critical to identify and develop potential therapeutic agents capable of promoting corneal re-epithelialization to accelerate the wound healing process. The focus of this review is to examine what is known regarding the cellular and molecular mechanisms needed to maintain epithelial homeostasis and how it goes awry in diabetes.