Dry eye disorders are becoming more common due to many causes, including an aging population, increased pollution, and postrefractive surgery. Current treatments include
artificial tears;
gels;
lubricants; tear duct plugs; and
anti-inflammatory agents such as
steroids,
doxycycline, and
cyclosporine. For more severe forms of the disease, serum tears and scleral
contact lenses are employed. Despite these
therapies, successful resolution of the problem is limited because none of these treatments fully addresses the underlying causes of
dry eye to promote ocular surface repair.
Thymosin β4 (Tβ4), a small, naturally occurring
protein, promotes complete and faster corneal healing than saline alone or prescription agents (
doxycycline and
cyclosporine) in various animal models of
eye injury. In human trials, it improves both the signs and symptoms of moderate to severe
dry eye with effects lasting beyond the treatment period. This review will cover the multiple activities of Tβ4 on cell migration,
inflammation, apoptosis, cytoprotection, and gene expression with a focus on mechanisms of cell migration, including laminin-332 synthesis and degradation, that account for this paradigm-shifting potential new treatment for
dry eye disorders. We will also speculate on additional mechanisms that might promote eye repair based on data from other tissue injury models. Such studies provide the rationale for use of Tβ4 in other types of
eye disorders beyond
dry eye. Finally, we will identify the gaps in our knowledge and propose future research avenues.