Ocular surface epithelial cell apoptosis

Apoptosis of ocular surface epithelial cells refers to the programmed cell death of corneal and conjunctival epithelial cells, a process pivotal for the maintenance and pathology of the ocular surface[1][6]. This form of cell death is involved in normal tissue homeostasis but can be accelerated in response to environmental triggers such as ultraviolet radiation, hyperosmolarity (dry eye), or pharmacological exposure (corticosteroids)[1][2][4]. Mechanistically, apoptosis is driven by activation of potassium channels leading to K⁺ efflux, caspase activation, and mitochondrial signaling, and is detectable by molecular biomarkers such as TUNEL staining and caspase cleavage[2][4][6]. Dysregulated or excessive apoptosis contributes to diseases like dry eye and keratoconjunctivitis sicca and therefore represents an indirect therapeutic target[3][6]. However, because this is a process rather than a discrete molecular entity, anti-apoptotic therapies target upstream signaling pathways or environmental triggers rather than the apoptotic machinery itself[2][3][4].

Other names

epithelial cell apoptosis of ocular surfacecorneal epithelial apoptosisconjunctival epithelial cell apoptosis

Activation of K⁺ channels leading to K⁺ efflux and cell death upon stress (e.g., UV, hyperosmolarity). Glucocorticoid-induced apoptosis via intrinsic pathway and mitochondrial ROS. Inflammatory cytokine increase, caspase activation.