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. 2003 Jun 15;111(12):1817–1819. doi: 10.1172/JCI18927

Figure 1.

Figure 1

Retinal neovascularization is the result of hypoxia-induced damage to the neural retina and its capillaries (a). Following investigation of the effects of hypoxia in the presence and absence of IR/IGF-1R on retinal vascularization, Kondo et al. (6) found that under normoxic condition (b), the retinas of mice develop normally in the absence of endothelial IR/IGF-1R. Presumably, sufficient growth factors (e.g., VEGF) are present to facilitate normal development. Under conditions of relative hypoxia and in the presence of endothelial IR/IGF-1R (c), VEGF, eNOS, and ET-1 are increased, leading to extra-retinal neovascularization. Under conditions of relative hypoxia and in the absence of endothelial IR/IGF-1R (d), VEGF, eNOS, and ET-1 are reduced, possibly due to impaired HIF-1 activation or reduced PI3K activity related to IG/IGF-1R. Reduced neovascularization results from less IR/IGF-IR input.