Diabetic Retinopathy

Like AMD, diabetic retinopathy represents a serious public health problem. It is the leading cause of blindness in of individuals between the ages of 25 and 74 in the United States (National Eye Institute, 2005), a segment of the population that makes up the majority of the workforce.

Long-term exposure to elevated blood glucose levels causes damage to pericytes, small cells that surround and support the capillaries of the retinal vascular bed (Resnikoff et al., 2002). Loss of pericytes leads to focal weak spots developing along retinal vascular walls. These weak areas bulge outward, forming microa-neurysms, which leak (causing retinal edema) and eventually burst (causing retinal hemorrhage). This stage of diabetic retinopathy is called background or non-proliferative retinopathy because most diabetics develop at least mild microvascu-lar changes even with relatively good long-term blood glucose control. But the disease does not always stop there. If enough small vessels are affected, retinal tissue distal to these ruptured microaneurysms are deprived of blood and oxygen, and therefore become ischemic. Retinal ischemia promotes retinal angiogenesis, and hence "proliferative" diabetic retinopathy ensues. This form of the disease is far more visually debilitating because these patches of fibrovascular proliferation are hemorrhagic and often destroy normal retinal architecture in their effort to "rescue" distal ischemic tissue beds.

VEGF drives diabetic retinopathy. In a mouse model of diabetes, the expression of VEGF mRNA was more than three-fold higher in diabetic eyes than in non-diabetic eyes (Qaum et al., 2001). Retinal vascular damage similar to diabetic retinopathy can be induced by injecting VEGF into primate eyes (Tolentino et al., 1996). In humans, vitreous VEGF levels are higher in patients with diabetic macular edema than in both normal subjects and diabetics without retinopathy (Funatsu et al., 2002). Increased VEGF levels have also been found in both the aqueous

(Aiello et al., 1994) and vitreous (Adamis et al., 1994) of human eyes with proliferative diabetic retinopathy.

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