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Proposed model for paracrine control of choroidal neovascularization via alterations in VEGF deposition within the RPE ECM. Hypoxia results in increased VEGF expression, and changes in the capacity of the RPE ECM to bind to VEGF. The increased VEGF-laden matrix may then selectively bind to VEGFR2 on endothelial and endothelial progenitor cells to facilitate the interaction with the ECM and ultimately, angiogenesis.
