Extracellular vesicles (EVs) are small membrane-bound particles that play a vital role in intercellular communication by facilitating the transfer of molecular cargo. In this review, we provide an overview of EV biology in corneal diseases, along with current approaches to therapeutic uses of EVs. Since EVs generally retain surface markers indicative of their cell of origin, they possess a degree of tissue specificity, which benefits drug delivery systems and highlights their potential as biomarkers to study disease processes. Further advances in technology and methodology will accelerate our understanding of EVs and help guide the field towards improved diagnostic techniques and therapeutic targets. We summarize EVs and their potential impact in medicine with a discussion of the limitations that remain in current approaches, as well as areas to focus on for future growth.

Corneal scarring is a result of unregulated fibrotic processes in wound healing, which causes visual impairment. Bioactive sphingolipids (SPLs) are known to modulate physiological processes that are central to wound healing. Of these bioactive SPLs, sphingosine-1-phosphate (S1P) is perhaps the most studied. Previous research has shown that knocking out sphingosine kinase 1 (Sphk1), which produces S1P, alters SPL species metabolism and improves wound healing in mice corneas. However, it is unknown how SphK1 knockout (SphK1^-/-) affects SPL metabolism during stages of corneal wound healing. Following an alkali burn procedure on wild-type (WT) and SphK1^-/- mice, corneal lipidomic profiles in unburned corneas at 1, 7, 14, and 28 days post-injury (DPI) were measured. Significant differences in SPL species between genotypes, both in uninjured mouse corneas and during distinct stages of corneal burn healing, were observed. WT mice expressed burn healing stage-dependent modulation of SPL species, with decreased expression of most SPL species observed at 1 and 14 DPI. Interestingly, this wild-type SPL modulation was absent in most measured SPL species in the SphK1^-/- corneas. These findings provide evidence for a previously unknown modulatory role of SphK1 and S1P on the expression of SPLs during corneal wound healing.