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Updated: Feb 11, 2026

Coculture of Axotomized Rat Retinal Ganglion Neurons with Olfactory Ensheathing Glia, as an In Vitro Model of Adult Axonal Regeneration
Published on: November 2, 2020
Caspases in retinal ganglion cell death and axon regeneration
Chloe N Thomas1, Martin Berry1, Ann Logan1
1Neuroscience and Ophthalmology, Institute of Inflammation and Ageing, University of Birmingham, Birmingham, UK.
Abstract:
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.
Insights
Retinal ganglion cells (RGC) undergo apoptosis and pyroptosis via caspases, leading to vision loss. Inhibiting these caspases offers a potential therapeutic strategy for protecting RGCs and preserving vision.
Area of Science:
- Neuroscience
- Ophthalmology
- Cell Biology
Background:
- Retinal ganglion cells (RGCs) are crucial for vision but have limited regenerative capacity.
- RGC death contributes to permanent visual impairment in various optic neuropathies.
Purpose of the Study:
- To review the molecular mechanisms of caspase-dependent RGC death.
- To explore the therapeutic potential of targeting caspases for RGC protection.
Main Methods:
- Review of existing literature on RGC death pathways.
- Analysis of apoptotic and pyroptotic signaling in RGCs.
Main Results:
- Caspase-dependent apoptosis and pyroptosis are key mechanisms in RGC degeneration.
- Inhibiting caspases can protect RGCs from cell death.
Conclusions:
- Caspase signaling pathways are critical in RGC survival and death.
- Targeting apoptotic and inflammatory caspases presents a promising therapeutic avenue for vision preservation.
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