This is a mechanism module, not a specific disease. Disorder entries reference individual nodes via conforms_to (e.g., "glaucoma_optic_neuropathy#Retinal Ganglion Cell Apoptosis"). Conforming nodes should substitute the disorder-specific cause of raised outflow resistance (juxtacanalicular ECM accumulation in POAG, pupillary block/angle closure in angle-closure glaucoma, fibrillar exfoliation material in exfoliation glaucoma, MYOC/trabecular gene defects in juvenile glaucoma). Normal-tension glaucoma is a partial exception in which RGC loss occurs at statistically normal IOP.
Trabecular Meshwork Outflow Dysfunction
trigger
The trabecular meshwork in the iridocorneal angle is the principal drainage pathway for aqueous humor. Accumulation and reorganization of extracellular matrix in the juxtacanalicular tissue, loss of trabecular cellularity, and cytoskeletal stiffening increase resistance to aqueous outflow. This outflow dysfunction is the conserved initiating lesion across most glaucomas.
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Elevated Intraocular Pressure
Elevated Intraocular Pressure
amplifier
Increased resistance to aqueous humor drainage raises intraocular pressure. Elevated IOP is the principal modifiable risk factor for glaucoma and the proximate mechanical stressor transmitted to the optic nerve head and lamina cribrosa, where the retinal ganglion cell axons exit the eye.
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Retinal Ganglion Cell Apoptosis
Retinal Ganglion Cell Apoptosis
central effector
Pressure-related mechanical stress at the optic nerve head, combined with oxidative stress, impaired axonal transport, and neurotrophin deprivation, triggers apoptosis of retinal ganglion cells. This is the central effector step of glaucomatous neurodegeneration and is shared across glaucoma subtypes.
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Optic Nerve Degeneration and Neuroinflammation
Optic Nerve Degeneration and Neuroinflammation
effector
Progressive retinal ganglion cell loss is accompanied by optic nerve axon degeneration and a glial neuroinflammatory response that further accelerates neurodegeneration. Oxidative DNA damage accumulating in the degenerating tissue amplifies this neuroinflammatory drive.
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Progressive Glaucomatous Optic Neuropathy
Progressive Glaucomatous Optic Neuropathy
consequence
Cumulative retinal ganglion cell and axon loss produces the characteristic optic disc cupping, retinal nerve fiber layer thinning, and progressive, irreversible visual field loss that define glaucoma as a clinical entity.