Oxidative stress, hypoxia, and autophagy in the neovascular processes of age-related macular degeneration.
Age-related macular degeneration (AMD) is the leading cause of severe and irreversible loss of vision in the elderly in developed countries. AMD is a complex chronic neurodegenerative disease associated with many environmental, lifestyle, and genetic factors. Oxidative stress and the production of reactive oxygen species (ROS) seem to play a pivotal role in AMD pathogenesis. It is known that the macula receives the highest blood flow of any tissue in the body when related to size, and anything that can reduce the rich blood supply can cause hypoxia, malfunction, or disease. Oxidative stress can affect both the lipid rich retinal outer segment structure and the light processing in the macula. The response to oxidative stress involves several cellular defense reactions, for example, increases in antioxidant production and proteolysis of damaged proteins. The imbalance between production of damaged cellular components and degradation leads to the accumulation of detrimental products, for example, intracellular lipofuscin and extracellular drusen. Autophagy is a central lysosomal clearance system that may play an important role in AMD development. There are many anatomical changes in retinal pigment epithelium (RPE), Bruch's membrane, and choriocapillaris in response to chronic oxidative stress, hypoxia, and disturbed autophagy and these are estimated to be crucial components in the pathology of neovascular processes in AMD.
Faculty of Biology and Environmental Protection, Department of Molecular Genetics, University of Lodz, 90-236 Lodz, Poland.
Janusz
0000-0001-9539-9584
J
Blasiak
Department of Ophthalmology, Faculty of Medicine, University of Szeged, Szeged 6720, Hungary ; Stem Cells and Eye Research Laboratory, Department of Biochemistry and Molecular Biology, Medical and Health Science Center and Apoptosis and Genomics Research Group of the Hungarian Academy of Sciences, University of Debrecen, Debrecen 4010, Hungary.
Goran
0000-0003-2905-9252
G
Petrovski
Stem Cells and Eye Research Laboratory, Department of Biochemistry and Molecular Biology, Medical and Health Science Center and Apoptosis and Genomics Research Group of the Hungarian Academy of Sciences, University of Debrecen, Debrecen 4010, Hungary.
Zoltán
Z
Veréb
Department of Ophthalmology, Faculty of Medicine, University of Szeged, Szeged 6720, Hungary.
Andrea
A
Facskó
Department of Ophthalmology, Institute of Clinical Medicine, University of Eastern Finland, 70211 Kuopio, Finland ; Department of Ophthalmology, Kuopio University Hospital, 70211 Kuopio, Finland.
Kai
K
Kaarniranta
D000975:Antioxidants / Q000378:metabolism; D001343:Autophagy / Q000502:physiology; D006801:Humans; D000860:Hypoxia / Q000378:metabolism; D008268:Macular Degeneration / Q000378:metabolism / Q000503:physiopathology*; D009389:Neovascularization, Pathologic / Q000378:metabolism / Q000503:physiopathology; D018384:Oxidative Stress / Q000235:genetics*; D017382:Reactive Oxygen Species / Q000378:metabolism; D055213:Retinal Pigment Epithelium / Q000378:metabolism / Q000503:physiopathology*
D000975:Antioxidants; D017382:Reactive Oxygen Species