Abstract
Glaucoma is a group of optic neuropathies characterised by the degeneration of retinal ganglion cells, resulting in damage to the optic nerve head (ONH) and loss of vision in one or both eyes. Increased intraocular pressure (IOP) is one of the major aetiological risk factors in glaucoma, and is currently the only modifiable risk factor. However, 30–40% of glaucoma patients do not present with elevated IOP and still proceed to lose vision. The pathophysiology of glaucoma is therefore not completely understood, and there is a need for the development of IOP-independent neuroprotective therapies to preserve vision. Neuroinflammation has been shown to play a key role in glaucoma and, specifically, the NLRP3 inflammasome, a key driver of inflammation, has recently been implicated. The NLRP3 inflammasome is expressed in the eye and its activation is reported in pre-clinical studies of glaucoma. Activation of the NLRP3 inflammasome results in IL-1β processing. This pro inflammatory cytokine is elevated in the blood of glaucoma patients and is believed to drive neurotoxic inflammation, resulting in axon degeneration and the death of retinal ganglion cells (RGCs). This review discusses glaucoma as an inflammatory disease and evaluates targeting the NLRP3 inflammasome as a therapeutic strategy. A hypothetical mechanism for the action of the NLRP3 inflammasome in glaucoma is presented.
Highlights
Glaucoma is a neurodegenerative disease and the leading cause of irreversible blindness worldwide
Glaucoma is characterised by degeneration of the retinal ganglion cell (RGC) axons resulting in damage or remodelling of the optic nerve head (ONH), as evidenced by the characteristic clinical sign of optic disc cupping [4]
Elevated intraocular pressure (IOP) is the only modifiable risk factor in glaucoma, and IOP lowering therapies are unsuccessful in many patients
Summary
Glaucoma is a neurodegenerative disease and the leading cause of irreversible blindness worldwide. Glaucoma is characterised by degeneration of the retinal ganglion cell (RGC) axons resulting in damage or remodelling of the optic nerve head (ONH), as evidenced by the characteristic clinical sign of optic disc cupping [4]. These clinical manifestations lead to disruption of the visual pathway and vision loss in one or both eyes [5]. Approximately 30–40% of POAG patients exhibit a normal IOP, indicating that elevated IOP is not the sole causative factor of glaucoma [9]. There is an emerging body of evidence to support the role of inflammation in glaucoma pathogenesis [14,15]
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