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Review
. 2017:2017:3940241.
doi: 10.1155/2017/3940241. Epub 2017 Dec 19.

Ischemic Retinopathies: Oxidative Stress and Inflammation

José Carlos Rivera  1   2 , Rabah Dabouz  1 , Baraa Noueihed  1 , Samy Omri  1 , Houda Tahiri  1 , Sylvain Chemtob  1   2
Affiliations
Review

Ischemic Retinopathies: Oxidative Stress and Inflammation

José Carlos Rivera et al. Oxid Med Cell Longev. 2017.

Abstract

Ischemic retinopathies (IRs), such as retinopathy of prematurity (ROP), diabetic retinopathy (DR), and (in many cases) age-related macular degeneration (AMD), are ocular disorders characterized by an initial phase of microvascular changes that results in ischemia, followed by a second phase of abnormal neovascularization that may culminate into retinal detachment and blindness. IRs are complex retinal conditions in which several factors play a key role during the development of the different pathological stages of the disease. Increasing evidence reveals that oxidative stress and inflammatory processes are important contributors to the pathogenesis of IRs. Despite the beneficial effects of the photocoagulation and anti-VEGF therapy during neovascularization phase, the need to identify novel targets to prevent initial phases of these ocular pathologies is still needed. In this review, we provide an update on the involvement of oxidative stress and inflammation in the progression of IRs and address some therapeutic interventions by using antioxidants and anti-inflammatory agents.

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Figures

Figure 1
Figure 1
The effects of oxidant stress on premature retinal vasculature. The premature retina is relatively deficient in antioxidants. Consequently, oxidant stress is more likely to induce peroxidation and nitration that is cytotoxic to retinal microvasculature. Downstream mediators of peroxidation, notably the phospholipids PAF and LPA, the nonenzymatically derived prostanoids, isoprostanes, and nitration products such as trans-arachidonic acids (TAAs), are all cytotoxic to retinovascular endothelium, causing vasoobliteration. PLD: phospholipase D; PLA2: phospholipase A2; PM: plasma membrane; PGS: PG synthase; TXS: thromboxane synthase; TSP-1: thrombospondin-1.
Figure 2
Figure 2
The role of oxidative stress and inflammation in diabetic retinopathy. Hyperglycemia activates PKC, AGEs, polyol, and hexosamine pathways which contribute to oxidative stress and mitochondrial dysfunction leading to pericyte and endothelial cell apoptosis. Upregulation of inflammatory mediators results in cell death and BRB breakdown.
Figure 3
Figure 3
Scheme summarizing the risk factors of AMD, the link between oxidative stress and inflammatory factors involved in the pathogenesis of dry AMD and the current antioxidant/anti-inflammatory therapeutic trials and recommendations. CFH: complement factor H; CFB: complement factor B; C3: complement 3; APOE: apolipoprotein E; NADH: nicotinamide adenine dinucleotide H; SOD2: superoxide dismutase 2; ROS: reactive oxygen species; MCP1: monocyte chemotactic protein 1; CX3CL1: C-X3-C motif chemokine ligand 1; IL-1β: interleukine 1 beta; iNOS: inducible nitric oxide synthase; TNFα: tumor necrosis factor alpha; NRTI: nucleoside reverse transcriptase inhibitor; RPE: retinal pigment epithelium.
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