The impact of oxidative stress and inflammation on RPE degeneration in non-neovascular AMD

The retinal pigment epithelium (RPE) is a highly specialized, unique epithelial cell that interacts with photoreceptors on its apical side and with Bruch's membrane and the choriocapillaris on its basal side. Due to vital functions that keep photoreceptors healthy, the RPE is essential for main...

Full description

Saved in:
Bibliographic Details
Published in:Progress in retinal and eye research 2017-09, Vol.60, p.201-218
Main Authors: Datta, Sayantan, Cano, Marisol, Ebrahimi, Katayoon, Wang, Lei, Handa, James T.
Format: Article
Language:English
Subjects:
Age-related macular degeneration
Complement
Humans
Immunity, Innate - physiology
Inflammation
Macular Degeneration - etiology
Macular Degeneration - physiopathology
Mitochondria - physiology
Mitochondrial dynamics
Nrf2
Oxidative stress
Oxidative Stress - physiology
Phagocytosis - physiology
Retinal pigment epithelium
Retinal Pigment Epithelium - physiopathology
Risk Factors
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:The retinal pigment epithelium (RPE) is a highly specialized, unique epithelial cell that interacts with photoreceptors on its apical side and with Bruch's membrane and the choriocapillaris on its basal side. Due to vital functions that keep photoreceptors healthy, the RPE is essential for maintaining vision. With aging and the accumulated effects of environmental stresses, the RPE can become dysfunctional and die. This degeneration plays a central role in age-related macular degeneration (AMD) pathobiology, the leading cause of blindness among the elderly in western societies. Oxidative stress and inflammation have both physiological and potentially pathological roles in RPE degeneration. Given the central role of the RPE, this review will focus on the impact of oxidative stress and inflammation on the RPE with AMD pathobiology. Physiological sources of oxidative stress as well as unique sources from photo-oxidative stress, the phagocytosis of photoreceptor outer segments, and modifiable factors such as cigarette smoking and high fat diet ingestion that can convert oxidative stress into a pathological role, and the negative impact of impairing the cytoprotective roles of mitochondrial dynamics and the Nrf2 signaling system on RPE health in AMD will be discussed. Likewise, the response by the innate immune system to an inciting trigger, and the potential role of local RPE production of inflammation, as well as a potential role for damage by inflammation with chronicity if the inciting trigger is not neutralized, will be debated.
ISSN:1350-9462
1873-1635
DOI:10.1016/j.preteyeres.2017.03.002