The Role of the Reactive Oxygen Species and Oxidative Stress in the Pathomechanism of the Age-Related Ocular Diseases and Other Pathologies of the Anterior and Posterior Eye Segments in Adults - PubMed (original) (raw)

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Małgorzata Nita et al. Oxid Med Cell Longev. 2016.

Abstract

The reactive oxygen species (ROS) form under normal physiological conditions and may have both beneficial and harmful role. We search the literature and current knowledge in the aspect of ROS participation in the pathogenesis of anterior and posterior eye segment diseases in adults. ROS take part in the pathogenesis of keratoconus, Fuchs endothelial corneal dystrophy, and granular corneal dystrophy type 2, stimulating apoptosis of corneal cells. ROS play a role in the pathogenesis of glaucoma stimulating apoptotic and inflammatory pathways on the level of the trabecular meshwork and promoting retinal ganglion cells apoptosis and glial dysfunction in the posterior eye segment. ROS play a role in the pathogenesis of Leber's hereditary optic neuropathy and traumatic optic neuropathy. ROS induce apoptosis of human lens epithelial cells. ROS promote apoptosis of vascular and neuronal cells and stimulate inflammation and pathological angiogenesis in the course of diabetic retinopathy. ROS are associated with the pathophysiological parainflammation and autophagy process in the course of the age-related macular degeneration.

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Figures

Figure 1

Figure 1

Schematic overview of the harmful influence of ROS and the oxidative stress on the trabecular meshwork structure and its function in glaucoma. ROS, reactive oxygen species; mtDNA, mitochondrial deoxyribonucleic acid; TM, trabecular meshwork; ECM, extracellular matrix; NF-_κ_B, nuclear factor-_κ_B; ROS/ONOO−, reactive oxygen species/peroxynitrite; IOP, intraocular pressure.

Figure 2

Figure 2

Schematic overview of the influence of ROS and the oxidative stress on the retina and the optic nerve head changes in the course of glaucomatous neurodegeneration. IOP, intraocular pressure; ROS, reactive oxygen species; mtDNA, mitochondrial deoxyribonucleic acid; RGCs, retinal ganglion cells; BECN1/PtdIns3K, Beclin 1/phosphatidylinositol 3-kinase; AGEs, advanced glycation end products; ONH, optic nerve head; TNF-α, tumor necrosis factor alpha; NO, nitric oxide; AGE/RAGE, advanced glycation end product/receptor for advanced glycation end product; MMPs, matrix metalloproteinases; ECM, extracellular matrix.

Figure 3

Figure 3

Schematic overview of the ROS influence on the development of microvascular complications, neurodegeneration, and pathological angiogenesis in the course of diabetic retinopathy. mtDNA, mitochondrial deoxyribonucleic acid; ROS, reactive oxygen species; Sirt6, the name of a nuclear chromatin-bound protein; RAS, renin-angiotensin system; BDNF, brain-derived neurotrophic factor; PKC, the protein kinase C, AGEs, advanced glycation end products; NF-_κ_B, nuclear factor-_κ_B; TNF-α, tumor necrosis factor alpha; IL-6, IL-8, interleukins 6 and 8; COX-2, cyclooxygenase 2; ICAM-1, intercellular adhesion molecule 1; MCP-1, monocyte chemoattractant protein 1; VEGF, vascular endothelial growth factor; PHDs, prolyl hydroxylases; HIF-1, hypoxia-inducible factor-1; SCDF-1, stromal cell derived factor-1; RAAS, rennin-angiotensin-aldosterone system; NADPH-oxidase, nicotinamide adenine dinucleotide phosphate-oxidase.

Figure 4

Figure 4

Schematic overview of the ROS influence on the development of early and advanced forms of age-related macular degeneration. PUFA, polyunsaturated fatty acid; A2E, a component of retinal pigmented epithelial cell (RPE) lipofuscin; ROS, reactive oxygen species; mtDNA, mitochondrial deoxyribonucleic acid; ECM, extracellular matrix; PECAM-1, platelet endothelial cell adhesion molecule; VEGF, vascular endothelial growth factor; SD, soft drusen; GA/AMD, geographic atrophy/age-related macular degeneration; CNV/AMD, choroidal neovascularization/age-related macular degeneration.

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