Diabetic Macular Edema: Pathophysiology and Novel Therapeutic Targets

Diabetic macular edema (DME) is the major cause of vision loss in diabetic persons. Alteration of the bloode retinal barrier is the hallmark of this disease, characterized by pericyte loss and endothelial cellecell junction breakdown. Recent animal and clinical studies strongly indicate that DME is an inflammatory disease. Multiple cytokines and chemokines are involved in the pathogenesis of DME, with multiple cellular involvement affecting the neurovascular unit. With the introduction of antievascular endothelial growth factor (VEGF) agents, the treatment of DME has been revolutionized, and the indication for laser therapy has been limited. However, the response to anti-VEGF drugs in DME is not as robust as in proliferative diabetic retinopathy, and many patients with DME do not show complete resolution of fluid despite multiple intravitreal injections. Potential novel therapies targeting molecules other than VEGF and using new drugdelivery systems currently are being developed and evaluated in clinical trials. (C) 2015 by the American Academy of Ophthalmology.