In search of new targets for retinal neuroprotection: is there a role for autophagy?

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• 作者：Rossella Russo¹ ; ^{rossella.russo@unical.it} ; ^{russors@hotmail.com} ; Laura Berliocchi² ; Annagrazia Adornetto¹ ; Diana Amantea¹ ; Carlo Nucci³ ; Cristina Tassorelli⁴ ; Luigi Antonio Morrone¹ ; ⁵ ; Giacinto Bagetta¹ ; ⁵ ; Maria Tiziana Corasaniti²
• 刊名：Current Opinion in Pharmacology
• 出版年：2013
• 出版时间：February, 2013
• 年：2013
• 卷：13
• 期：1
• 页码：72-77
• 全文大小：698 K

文摘

Autophagy is a highly conserved catabolic pathway in which proteins and organelles are engulfed by vacuoles that are targeted to lysosomes for degradation. Defects in the autophagic machinery have been described in several neurodegenerative diseases uncovering the tight dependency of neuronal survival on the efficiency of the autophagic process. Despite the large amount of literature investigating autophagy in a number of pathological conditions our knowledge of its role in glaucoma neurodegeneration is just beginning.

However, recent experimental data revealing that autophagy modulation occurs in retinal ganglion cells (RGCs) under glaucoma-related stressing conditions support the hypothesis that dysfunctional autophagy might underlie the process leading to RGC death.

Although our understanding of the role of autophagy in glaucoma is still developing, there is the possibility that neuroprotection may be achieved by modulating autophagy. This would be a promising approach as it could lead to the much-sought development of alternative therapeutic strategies to prevent visual loss in glaucoma.