Caspases in retinal ganglion cell death and axon regeneration

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Caspases in retinal ganglion cell death and axon regeneration. / Thomas, Chloe; Berry, Martin; Logan, Ann; Blanch, Richard; Ahmed, Zubair.

In: Cell Death Discovery, Vol. 3, 17032, 03.07.2017.

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@article{0b32f2b46f8c44fe9fe3f8ce0fa5a48a,
title = "Caspases in retinal ganglion cell death and axon regeneration",
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.",
keywords = "apoptosis , cell death in the nervous system",
author = "Chloe Thomas and Martin Berry and Ann Logan and Richard Blanch and Zubair Ahmed",
year = "2017",
month = jul
day = "3",
doi = "10.1038/cddiscovery.2017.32",
language = "English",
volume = "3",
journal = "Cell Death Discovery",
issn = "2058-7716",
publisher = "Nature Publishing Group",

}

RIS

TY - JOUR

T1 - Caspases in retinal ganglion cell death and axon regeneration

AU - Thomas, Chloe

AU - Berry, Martin

AU - Logan, Ann

AU - Blanch, Richard

AU - Ahmed, Zubair

PY - 2017/7/3

Y1 - 2017/7/3

N2 - 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.

AB - 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.

KW - apoptosis

KW - cell death in the nervous system

U2 - 10.1038/cddiscovery.2017.32

DO - 10.1038/cddiscovery.2017.32

M3 - Review article

C2 - 29675270

VL - 3

JO - Cell Death Discovery

JF - Cell Death Discovery

SN - 2058-7716

M1 - 17032

ER -