Abstract
Corneal fibrosis develops in response to injury, infection, postsurgical complications, or underlying systemic disease that disrupts the homeostasis of the tissue leading to irregular extracellular matrix deposition within the stroma. The mechanisms that regulate corneal scarring are focused heavily on the canonical transforming growth factor-β pathway and relevant activators, and their role in promoting myofibroblast differentiation. In this paper, we discuss the biochemical pathways involved in corneal fibrosis in the context of different injury models-epithelial debridement, superficial keratectomy, and penetrating incision. We elaborate on the interplay of the major pro-fibrotic factors involved in corneal scar development (e.g., transforming growth factor-β1, thrombospondin-1, and ανβ6), and explore a novel role for extracellular vesicles secreted by the wounded epithelium and the importance of the basement membrane.
Highlights
Corneal scarring may be caused by infection, injury, or disease and result in restricted passage of light that reaches the retina, often leading to detrimental effects on visual acuity
We focus on wound models using mice, given the broad availability of knockout models to study the role of specific factors involved in corneal wound healing
The potentiality for corneal scar development is largely dependent on the integrity of the epithelial and endothelial layers and their respective basement membranes, which influence the penetrance of pro-fibrotic factors [e.g., transforming growth factor-β (TGF-β), thrombospondin-1 (TSP1), and extracellular vesicles (EVs)] into the stroma (Fig. 1)
Summary
Corneal scarring may be caused by infection, injury, or disease and result in restricted passage of light that reaches the retina, often leading to detrimental effects on visual acuity. The potentiality for corneal scar development is largely dependent on the integrity of the epithelial and endothelial layers and their respective basement membranes, which influence the penetrance of pro-fibrotic factors [e.g., transforming growth factor-β (TGF-β), thrombospondin-1 (TSP1), and extracellular vesicles (EVs)] into the stroma (Fig. 1).
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