Hypoxia-induced oxidative stress in ischemic retinopathy - PubMed (original) (raw)

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Hypoxia-induced oxidative stress in ischemic retinopathy

Suk-Yee Li et al. Oxid Med Cell Longev. 2012.

Abstract

Oxidative stress plays a crucial role in the pathogenesis of retinal ischemia/hypoxia, a complication of ocular diseases such as diabetic retinopathy (DR) and retinopathy of prematurity (ROP). Oxidative stress refers to the imbalance between the production of reactive oxygen species (ROS) and the ability to scavenge these ROS by endogenous antioxidative systems. Free radicals and ROS are implicated in the irreversible damage to cell membrane, DNA, and other cellular structures by oxidizing lipids, proteins, and nucleic acids. Anti-oxidants that can inhibit the oxidative processes can protect retinal cells from ischemic/hypoxic insults. In particular, treatment using anti-oxidants such as vitamin E and lutein, inhibition of nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase) or related signaling pathways, and administration of catalase and superoxide dismutase (SOD) are possible therapeutic regimens for DR, ROP, and other retinal ischemic diseases. The role of oxidative stress in the pathogenesis of DR and ROP as well as the underlying mechanisms involved in the hypoxia/ischemia-induced oxidative damage is discussed. The information provided will be beneficial in understanding the underlying mechanisms involved in the pathogenesis of the diseases as well as in developing effective therapeutic interventions to treat oxidative stress-induced damages.

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Figures

Figure 1

Figure 1

Schematic showing the relationship between oxidative stress and DR. The four major mechanisms involved in DR: increased polyol pathway flux, increased AGE formation, activation of PKC pathway, and increased hexosamine pathway flux results in I/R and increased production of ROS/RNS, thereby changing the levels of JNK/p38 MAPK, PARP, and NF_κ_B, increasing lipid peroxidation as well as leading to mitochondrial dysfunction.

Figure 2

Figure 2

Schematic showing the relationship of I/R, oxidative stress, and ROP. I/R causes overproduction of ROS/RNS. The resulting changes in levels of JAK/STAT, nitro-oxidation, and VEGF/IGF-1 contribute to pathogenesis of ROP.

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