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Review
. 2020 Mar 4:8:121.
doi: 10.3389/fcell.2020.00121. eCollection 2020.

The Role of Autophagy in Glaucomatous Optic Neuropathy

Affiliations
Review

The Role of Autophagy in Glaucomatous Optic Neuropathy

Annagrazia Adornetto et al. Front Cell Dev Biol. .

Abstract

Autophagy is a conserved lysosomal-dependent pathway responsible for the degradation of cytoplasmic macromolecules. Based on the mechanism of cargo delivery to lysosomes, mammalian cells can undergo micro, macro, and chaperone-mediated autophagy. Other than physiological turnover of proteins and organelles, autophagy regulates cellular adaptation to different metabolic states and stressful conditions by allowing cellular survival or, when overactivated, participating to cell death. Due to their structure and function, neurons are highly dependent on autophagy efficiency and dysfunction of the pathway has been associated with neurodegenerative disorders. Glaucomatous optic neuropathies, a leading cause of blindness, are characterized by the progressive loss of a selective population of retinal neurons, i.e., the retinal ganglion cells (RGCs). Here we review the current literature on the role of autophagy in the pathogenic process that leads to the degeneration of RGC in various experimental models of glaucoma exploring the modulation of the pathway as a potential therapeutic intervention.

Keywords: CMA; LC3; autophagy; glaucoma; mitophagy; p62; retina; retinal ganglion cells.

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Figures

FIGURE 1
FIGURE 1
Element of the visual pathway. (Optic nerve Head, ONH; Lateral Geniculate Nucleus, LGN).

References

    1. Almasieh M., Wilson A. M., Morquette B., Cueva Vargas J. L., Di Polo A. (2012). The molecular basis of retinal ganglion cell death in glaucoma. Prog. Retin. Eye Res. 31 152–181. 10.1016/j.preteyeres.2011.11.002 - DOI - PubMed
    1. Chen G., Tang L., Wei W., Li Z., Li Y., Duan X., et al. (2016). mTOR regulates neuroprotective effect of immunized CD4+Foxp3+ T cells in optic nerve ischemia. Sci. Rep. 6:37805. 10.1038/srep37805 - DOI - PMC - PubMed
    1. Cianfanelli V., D’orazio M., Cecconi F. (2015). AMBRA1 and BECLIN 1 interplay in the crosstalk between autophagy and cell proliferation. Cell Cycle 14 959–963. 10.1080/15384101.2015.1021526 - DOI - PMC - PubMed
    1. Coughlin L., Morrison R. S., Horner P. J., Inman D. M. (2015). Mitochondrial morphology differences and mitophagy deficit in murine glaucomatous optic nerve. Invest. Ophthalmol. Vis. Sci. 56 1437–1446. 10.1167/iovs.14-16126 - DOI - PMC - PubMed
    1. Cuervo A. M., Dice J. F. (2000). Unique properties of lamp2a compared to other lamp2 isoforms. J. Cell Sci. 113(Pt 24), 4441–4450. - PubMed

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