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Review
. 2021 Jul 27;22(15):7994.
doi: 10.3390/ijms22157994.

Risk Factors for Retinal Ganglion Cell Distress in Glaucoma and Neuroprotective Potential Intervention

Stefania Vernazza  1 , Francesco Oddone  2 , Sara Tirendi  1   3 , Anna Maria Bassi  1   3
Affiliations
Review

Risk Factors for Retinal Ganglion Cell Distress in Glaucoma and Neuroprotective Potential Intervention

Stefania Vernazza et al. Int J Mol Sci. .

Abstract

Retinal ganglion cells (RGCs) are a population of neurons of the central nervous system (CNS) extending with their soma to the inner retina and with their axons to the optic nerve. Glaucoma represents a group of neurodegenerative diseases where the slow progressive death of RGCs results in a permanent loss of vision. To date, although Intra Ocular Pressure (IOP) is considered the main therapeutic target, the precise mechanisms by which RGCs die in glaucoma have not yet been clarified. In fact, Primary Open Angle Glaucoma (POAG), which is the most common glaucoma form, also occurs without elevated IOP. This present review provides a summary of some pathological conditions, i.e., axonal transport blockade, glutamate excitotoxicity and changes in pro-inflammatory cytokines along the RGC projection, all involved in the glaucoma cascade. Moreover, neuro-protective therapeutic approaches, which aim to improve RGC degeneration, have also been taken into consideration.

Keywords: degeneration; glaucoma; neuroinflammation; neuroprotection; retinal ganglion cells.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Risk factors contributing to RGC distress in glaucoma: the mechanisms implicated in RGC damage include deficiency in neurotrophic elements, glutamate excitotoxicity, hypoxia and ischemia, impairment of mitochondria functions, oxidative and nitrosative stress, alterations in axonal transport and in synaptic signals, unstructured proteins, apoptosis and other death mechanisms which can lead to premature senescence, and inflammation cascade which induce the activation of glial cells with consequent gliosis.The pathways, triggered by each risk factor, often result to be strictly interrelated, contributing to amplifying RGC distress in an irreversible way.
Figure 2
Figure 2
The Complement pathway: three pathways activate the Complement cascade, and they converge within this.
Figure 3
Figure 3
Neuroprotective mechanisms for preventing and slowing down RGC diseases.
See this image and copyright information in PMC

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