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. 2010 Jul 27;16(11-12):535–542. doi: 10.2119/molmed.2010.00070

Figure 1.

Figure 1

Schematic presentation depicting the role of ER stress in the pathogenesis of neovascular AMD. Several AMD risk factors trigger ER stress and activate UPR signaling via IRE1, PERK and ATF6/CREBH transducers. UPR induces the expression of stress resistance components, but excessive and prolonged insults can trigger the expression of VEGF, CHOP, CASP4 and NF-κB, evoking neovascularization and pathological changes in the macula region. Only the pathways known to be present in human RPE cells have been included.