Cellular and molecular events in corneal wound healing: significance of lipid signalling

Alterations in the normal healing process after corneal injury can produce undesirable outcomes that range from corneal haze to ulceration and perforation. Lipids play important roles in the complex inflammatory processes that occur after corneal wounding. While some lipid mediators, such as the lipoxygenase derivatives of arachidonic acid, 12-hydroxyeicosatetraenoic acid (12[S]-HETE and 15[S]-HETE), act as second messengers to promote cell proliferation and are possibly involved in the synthesis of other molecules that suppress inflammation, others, such as platelet-activating factor (PAF), exert their actions through specific receptors, play key roles during sustained corneal inflammation (as might occur with chemical burns), and contribute to tissue destruction and neovascularization. PAF is also a strong inducer of selective metalloproteinases (MMPs) that degrade the extracellular matrix. The use of a new PAF antagonist has shown great promise for the treatment of diffuse lamellar keratitis (DLK) and alkali-burned corneas.