The research progress on the molecular mechanism of corneal cross-linking in keratoconus treatment

Keratoconus (KC) is a corneal anomaly that is manifested in a limited cone-like bulge with corneal thinning. Many molecules in the cornea change during the development of KC, including various components of the extracellular matrix, cytokines, cell connection, and cell adhesion-related proteins. Several treatment options are available, with corneal cross-linking (CXL) being the treatment of choice for early KC. However, postoperative complications have been reported in some CXL patients, mainly caused by corneal epithelial resection. Despite the fact that some novel approaches have helped to reduce some of the initial post-operative issues, their effectiveness seems to be inferior to that of the original CXL. To keep effectiveness while avoiding these negative effects, it is necessary to study the mechanism of CXL in KC treatment at the molecular level. This article provides a review of the molecular mechanism of CXL in the treatment of KC from four aspects: enzyme activity, signal transduction pathway, corneal-related proteins, and other KC-related molecules, further confirming the feasibility of CXL treatment of KC, providing new ideas for improving CXL.

Automated summary

Keratoconus (KC) is a corneal anomaly characterized by a cone-like bulge and thinning of the cornea. Corneal cross-linking (CXL) is the preferred treatment option for early KC, but postoperative complications have been reported. To maintain effectiveness while avoiding negative effects, studying the molecular mechanism of CXL in KC treatment is necessary.