Interplay between reactive oxygen species and autophagy in the course of age-related macular degeneration

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Date

2020-09-25

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Publisher

IfADo - Leibniz Research Centre for Working Environment and Human Factors, Dortmund

Abstract

Pathological biomolecules such as lipofuscin, methylglyoxal-modified proteins (the major precursors of advanced glycationend products), misfolding protein deposits and dysfunctional mitochondria are source of oxidative stress and act as strong autophagic stimulators in age-related macular degeneration. Disturbed autophagy accelerates progression of the disease, since it leads to retinal cells’ death and activates inflammation by the interplay with the NLRP3 inflammasome complex. Vascular dysfunction and hypoxia, as well as circulating autoantibodies against autophagy regulators (anti-S100A9, anti-ANXA5, and anti-HSPA8, A9 and B4) compromise an autophagy-mediated mechanism as well. Metformin, the autophagic stimulator, may act as a senostatic drug to inhibit the senescent phenotype in the age-related macular degeneration. PGC-1α , Sirt1 and AMPK represent new therapeutic targets for interventions in this disease.

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Keywords

Reactive oxygen species, Oxidative stress, Autophagy, Age-related macular degeneration, Retina disease, Ophthalmology

Citation

Nita, M., & Grzybowski, A. (2020). Interplay between reactive oxygen species and autophagy in the course of age-related macular degeneration. EXCLI Journal, 19, 1353-1371. https://doi.org/10.17179/excli2020-2915