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Changing the fate of retinal ganglion cells following retinal ischemia: is autophagy the way?
Author(s) -
Russo R.,
Varano G.P.,
Adornetto A.,
Nazio F.,
Corasaniti M.T.,
Nucci C.,
Bagetta G.
Publication year - 2017
Publication title -
acta ophthalmologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.534
H-Index - 87
eISSN - 1755-3768
pISSN - 1755-375X
DOI - 10.1111/j.1755-3768.2017.03521
Subject(s) - autophagy , retinal , neuroprotection , retinal ganglion cell , microbiology and biotechnology , ischemia , programmed cell death , glaucoma , intraocular pressure , biology , retina , medicine , neuroscience , ophthalmology , apoptosis , biochemistry
Summary Autophagy is a highly conserved catabolic pathway for cell components to be degraded through the lysosomes and recycled under normal and stressful circumstances. The involvement of autophagy has been proven in several models of neurodenegerative diseases; however, its role in the neurodegenerative process occurring in retinal ganglion cells ( RGC s) exposed to glaucoma‐related stimuli is still controversial. Here we show that retinal ischemia induced by acute elevation of intraocular pressure ( IOP ) is associated with a dynamic, biphasic, modulation of the autophagic pathway, characterized by an initial upregulation of the process, which is followed by a reduced efficiency. Increased RGC death was reported in mice with partial genetic autophagy impairment ( AMBRA 1 +/‐ ) and subjected to retinal ischemia. Conversely, boosting basal autophagy, either by caloric restriction or pharmacological treatment, improved RGC survival suggesting that the catabolic pathway can be targeted to achieve neuroprotection.