Caspases in retinal ganglion cell death and axon regeneration

Chloe Thomas, Martin Berry, Ann Logan, Richard Blanch, Zubair Ahmed

Research output: Contribution to journalReview articlepeer-review

28 Citations (Scopus)
136 Downloads (Pure)


Retinal ganglion cells (RGC) are terminally differentiated CNS neurons that possess limited endogenous regenerative capacity after injury and thus RGC death causes permanent visual loss. RGC die by caspase-dependent mechanisms, including apoptosis, during development, after ocular injury and in progressive degenerative diseases of the eye and optic nerve, such as glaucoma, anterior ischemic optic neuropathy, diabetic retinopathy and multiple sclerosis. Inhibition of caspases through genetic or pharmacological approaches can arrest the apoptotic cascade and protect a proportion of RGC. Novel findings have also highlighted a pyroptotic role of inflammatory caspases in RGC death. In this review, we discuss the molecular signalling mechanisms of apoptotic and inflammatory caspase responses in RGC specifically, their involvement in RGC degeneration and explore their potential as therapeutic targets.

Original languageEnglish
Article number17032
JournalCell Death Discovery
Publication statusPublished - 3 Jul 2017


  • apoptosis
  • cell death in the nervous system


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