Targeting the NLRP3 Inflammasome in Glaucoma

Sophie Coyle, Mohammed Naeem Khan, Melody Chemaly, Breedge Callaghan, Chelsey Doyle, Colin E. Willoughby, Sarah D. Atkinson, Meredith Gregory-Ksander, Victoria McGilligan

Research output: Contribution to journalReview articlepeer-review

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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.
Original languageEnglish
Article numbere1239
Pages (from-to)1-14
Number of pages14
JournalBiomolecules
Volume11
Issue number8
Early online date19 Aug 2021
DOIs
Publication statusE-pub ahead of print - 19 Aug 2021

Keywords

  • NLRP3 inflammasome
  • glaucoma
  • RGC (retinal ganglion cells)
  • inflammation

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