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

Authors

  • Małgorzata Nita Domestic and Specialized Medicine Centre “Dilmed” Katowice, Poland, E-mail: m.nita@wp.pl
  • Andrzej Grzybowski Department of Ophthalmolgy, Medical Faculty, University of Warmia and Mazury, Olsztyn, Poland; Institute for Research in Ophthalmology, Gorczyczewskiego 2/3, 61-553 Poznań, Poland, E-mail: ae.grzybowski@gmail.com

DOI:

https://doi.org/10.17179/excli2020-2915

Keywords:

reactive oxygen species, oxidative stress, autophagy, age-related macular degeneration, retina disease, ophthalmology

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.

Downloads

Published

2020-09-25

How to Cite

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

Issue

Vol. 19 (2020)

Section

Review articles

License

Copyright (c) 2020 Małgorzata Nita, Andrzej Grzybowski

Creative Commons License

This work is licensed under a Creative Commons Attribution 4.0 International License.

Authors who publish in this journal agree to the following terms:

  • The authors keep the copyright and grant the journal the right of first publication under the terms of the Creative Commons Attribution license, CC BY 4.0. This licencse permits unrestricted use, distribution and reproduction in any medium, provided that the original work is properly cited.
  • The use of general descriptive names, trade names, trademarks, and so forth in this publication, even if not specifically identified, does not imply that these names are not protected by the relevant laws and regulations.
  • Because the advice and information in this journal are believed to be true and accurate at the time of publication, neither the authors, the editors, nor the publisher accept any legal responsibility for any errors or omissions presented in the publication. The publisher makes no guarantee, express or implied, with respect to the material contained herein.
  • The authors can enter into additional contracts for the non-exclusive distribution of the journal's published version by citing the initial publication in this journal (e.g. publishing in an institutional repository or in a book).