[2] By the end of eye development an interconnected keratocyte network is established in the cornea, with dendrites of neighbouring cells contacting each other.
[10] After an injury to the cornea, some keratocytes undergo apoptosis, prompted by the signaling molecules secreted by the upper layers, such as IL1 alpha and TNF-alpha.
Other neighbouring keratocytes, when acted upon by the same molecules, become active, proliferate and start synthesizing matrix metalloproteinases that cause tissue remodeling.
As soon as the basement membrane of corneal epithelium is restored, TGF beta inflow into the stroma drastically decreases and myofibroblasts disappear, after which the remaining activated keratocytes continue for some time to reshape the extracellular matrix, secreting IL1-alpha in order to maintain their "repair phenotype".
[2] Apoptosis is observed after eye operations, including keratotomy and laser surgery,[13] and may play a role in the development of post-surgery complications.
According to comparative research, their functions drastically diverge from the norm in keratoconus, the most frequent form of corneal dystrophy.
[15] According to one study, patient's keratocytes have decreased levels of one of the alcohol dehydrogenase subforms,[14] they secrete significantly less superoxide dismutase 3, according to another.