Limbal epithelial stem cell–associated pathways (LESC pathways)

Limbal epithelial stem cell (LESC) associated pathways represent a complex network of signaling systems, including Wnt/beta-catenin, Notch, TGF-beta/BMP, and Sonic Hedgehog, that maintain the regenerative capacity of the corneal surface (Di Girolamo et al., 2009). These pathways are primarily active within the limbal niche, a specialized microenvironment at the junction of the cornea and sclera that protects LESCs from differentiation and environmental stress (Notara et al., 2010). The primary biological function of these pathways is to regulate the balance between LESC self-renewal and the generation of transient amplifying cells required for corneal homeostasis. Dysregulation or physical destruction of these pathways leads to Limbal Stem Cell Deficiency (LSCD), a condition characterized by conjunctivalization, neovascularization, and chronic inflammation of the cornea (Pellegrini et al., 2001). While not a single molecular target, specific components of these pathways are targeted by therapies such as Cenegermin (recombinant human nerve growth factor), which promotes LESC proliferation and healing via the TrkA receptor (Bonini et al., 2018). Understanding these pathways is critical for developing advanced cell-based therapies and small-molecule drugs for ocular surface reconstruction.

Other names

Limbal stem cell signaling pathwaysCorneal epithelial stem cell regulatory networksLimbal niche signalingLESC regulatory pathways

Modulation of the limbal microenvironment and intracellular signaling cascades (e.g., Wnt, Notch, TGF-beta) to promote stem cell self-renewal, survival, and corneal epithelial repair.