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. Author manuscript; available in PMC: 2014 Mar 1.
Published in final edited form as: J Mol Med (Berl). 2013 Jan 18;91(3):311–321. doi: 10.1007/s00109-013-0993-5

Figure 5. Molecular pathogenesis of subretinal neovascularization (NV).

Figure 5

This schematic highlights several important molecular signals involved in subretinal NV. Oxidative stress in the retinal pigmented epithelium (RPE) and photoreceptors causes increased levels of HIF-1, which upregulates vasoactive gene products as described above. Retinal angiomatous proliferation (RAP) occurs if VEGF levels in photoreceptors are sufficiently high to cause an adequate gradient that reaches to the deep capillary bed of the retina. Choroidal NV occurs if there is elevation of VEGF and Angpt2 combined with perturbation of Bruch’s membrane and the RPE. The other HIF-1-responsive gene products fuel the process similar to the situation in retinal NV.