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Ophthalmology. 2015 Jul;122(7):1375-94. doi: 10.1016/j.ophtha.2015.03.024. Epub 2015 Apr 30.

Diabetic Macular Edema: Pathophysiology and Novel Therapeutic Targets.

Author information

1
Department of Surgery/Ophthalmology, University of New Mexico School of Medicine, Albuquerque, New Mexico; New Mexico VA Health Care System, Albuquerque, New Mexico. Electronic address: adas@unm.edu.
2
Department of Cell Biology and Physiology, University of New Mexico School of Medicine, Albuquerque, New Mexico.
3
T-Gen Institute, Phoenix, Arizona.

Abstract

Diabetic macular edema (DME) is the major cause of vision loss in diabetic persons. Alteration of the blood-retinal barrier is the hallmark of this disease, characterized by pericyte loss and endothelial cell-cell 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 anti-vascular 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 drug-delivery systems currently are being developed and evaluated in clinical trials.

PMID:
25935789
DOI:
10.1016/j.ophtha.2015.03.024
[Indexed for MEDLINE]
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