Caspases in retinal ganglion cell death and axon regeneration

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 prog...

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Bibliographic Details
Published inCell death discovery Vol. 3; no. 1; p. 17032
Main Authors Thomas, Chloe N, Berry, Martin, Logan, Ann, Blanch, Richard J, Ahmed, Zubair
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 03.07.2017
Springer Nature B.V
Nature Publishing Group
Subjects
631/378/1934
631/80/82/23
Apoptosis
Biochemistry
Biomedical and Life Sciences
Caspase
Cell Biology
Cell Cycle Analysis
Cell death
Central nervous system
Degeneration
Degenerative diseases
Diabetes mellitus
Diabetic neuropathy
Diabetic retinopathy
Eye
Glaucoma
Inflammation
Ischemia
Life Sciences
Multiple sclerosis
Optic nerve
Optic neuropathy
Regeneration
Retina
Retinal ganglion cells
Retinopathy
Review
review-article
Stem Cells
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Summary: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.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-3
content type line 23
ObjectType-Review-1
These two authors are joint senior authors.
ISSN:2058-7716
2058-7716
DOI:10.1038/cddiscovery.2017.32