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IUBMB Life 72 (9), 20242033

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It is generally acknowledged that the loss of endothelial NO is the central mechanism in the pathogenesis of endothelial dysfunction

Mice and humans that lack or overexpress MYOC have normal aqueous drainage and do not develop high IOP whereas mice expressing the human Tyr437His mutation in the olfactomedin domain develop elevated IOP and optic nerve damage that mirrors human glaucoma (21)

Third, therapeutic development will benefit from a biomarker-driven approach