Improving corneal nerve regeneration: initial results of a novel regenerative agent

Abstract

AbstractIt is well stablished that nerve deficit in the cornea leads to an imbalance in trophic factors required to maintain a healthy corneal tissue. This deficit is clinically manifested as impaired epithelial repair and wound healing, and eventually stromal scarring and ulceration, leading to a greater risk of transplant failure. Thus, corneal trophic environment must be restored by first promoting an adequate corneal nerve regeneration after transplant, although nowadays there is no approved neuro‐regenerative therapy for the cornea.A plethora of cytokines, chemokines and growth factors influence neuron survival and axon regeneration after lesion, most of them produced locally by Schwann cells at the distal nerve stump after nerve axotomy. In ARREST BLINDNESS work package 7, the efficacy of topical treatment with several cytokines, chemokines and trophic factors to promote corneal axon regeneration and the restoration of corneal sensory and trophic functions has been tested in an experimental model of surgically‐induced neurotrophic deficit, induced by performing a corneal stromal flap in the guinea‐pig. Using NGF as a positive control, protein neublastin, a member of the glial cell line derived neurotrophic factor family has been identified as the most effective factor to increase nerve regeneration after corneal lesion.(Supported by ARREST BLINDNESS, a project funded by the European Union’s Horizon 2020 Research and Innovation Programme under grant agreement No 667400)