Congenital limbal insufficiency includes aniridia, sclerocornea, and endocrinologic disturbances,
4 while acquired LSCD can arise from limbal injuries,
5 ocular surface immune disorders like Stevens Johnson syndrome,
6 long-term contact lens wearing,
7 and overexposure to detrimental substances,
8–11 A large variety of therapies, such as amniotic membrane transplantation, keratolimbal allograft, and transplantation of ex vivo expanded limbal epithelial cells, have been developed to treat LSCD and show inspiring clinical outcomes in patients.
12 However, the existing data are still limited by lack of understanding of the mechanisms involved in the occurrence of LSC failure. Until now, only one model of congenital LSCD can be found in the spontaneously vascularized corneas of
corn1 and
Pax6+/− mice with conjunctival invasion,
13 and heterozygosity for Pax6 deficiency (
Pax6+/− ) results in aniridia. Acute limbal destruction, as with severe chemical burns
14 and surgical removal of limbal tissues,
5 has been used for the induction of acquired LSCD in animals. However, the understanding of progressively developed LSCD is still limited by lack of animal models resulting from chronic and long-term stress over the ocular surface.