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Schematic of hypothesis that MCs contribute to GA. The working hypothesis is that choroidal MCs are activated by hypoxia-induced IL-33 production by RPE or CRP, AGEs, C3a or C5a, which are known to be elevated in AMD choroid. Upon activation and degranulation, tryptase is released into choroidal stroma and Bruch’s membrane. Tryptase can degrade choroidal stroma and Bruch’s membrane resulting in thinning of choroid and degeneration of RPE, which are hallmarks of GA.
