Abstract
Macular edema that results from blood–retinal barrier (BRB) breakdown is a cause of significant visual loss associated with a variety of ocular disorders. BRB breakdown is a complex process that is regulated by multiple factors and involves different mechanisms. A variety of therapeutic approaches have shown modest suppression of macular edema, but to obtain greater efficacy, it is likely that multiple molecules, operating through distinct mechanisms, may need to be targeted. Studies aimed at identifying key target molecules and the optimal strategies for inhibiting them are ongoing in several laboratories.