scholarly journals Involvement of Nrf2 in Ocular Diseases

2017 ◽  
Vol 2017 ◽  
pp. 1-18 ◽  
Author(s):  
Shehzad Batliwala ◽  
Christy Xavier ◽  
Yang Liu ◽  
Hongli Wu ◽  
Iok-Hou Pang

The human body harbors within it an intricate and delicate balance between oxidants and antioxidants. Any disruption in this checks-and-balances system can lead to harmful consequences in various organs and tissues, such as the eye. This review focuses on the effects of oxidative stress and the role of a particular antioxidant system—the Keap1-Nrf2-ARE pathway—on ocular diseases, specifically age-related macular degeneration, cataracts, diabetic retinopathy, and glaucoma. Together, they are the major causes of blindness in the world.

2021 ◽  
Vol 22 (3) ◽  
pp. 1296
Author(s):  
Yue Ruan ◽  
Subao Jiang ◽  
Adrian Gericke

Age-related macular degeneration (AMD) is a common irreversible ocular disease characterized by vision impairment among older people. Many risk factors are related to AMD and interact with each other in its pathogenesis. Notably, oxidative stress and choroidal vascular dysfunction were suggested to be critically involved in AMD pathogenesis. In this review, we give an overview on the factors contributing to the pathophysiology of this multifactorial disease and discuss the role of reactive oxygen species and vascular function in more detail. Moreover, we give an overview on therapeutic strategies for patients suffering from AMD.


Author(s):  
Mayuri Madanrao Jamunkar

Aging is the process of physiological psychological and social change in multidimensional aspects. As like the other structures of human body it is obvious and inevitable that the eye is also involved with various ailments leading to the manifestations of different ocular diseases in old age Among them important diseases are cataract, presbyopia, glaucoma, age related macular degeneration and diabetic retinopathy etc The pathological lesions in old age according to the ayurvedic concepts are swabhavika vhyadhis and it is difficult to cure completely so with an intension delay the Aging process Acharya recommend to start Rasayana therapy in middle age. Rasayana becomes more treat full and effective if it is preceded with suitable panchakarma. Triphala churna is advisable to all patients with diminished vision along with the honey and ghruta in unequal quantity which act as a Rasayana.    As geriatric problems are not attributed to a single cause, the treatment should be planned according to stage of the disease and the involved dosha on the basis of that we are treating the diseases by applying Classical ayurvedic measures along with kriyakalpa. Intake of Rasayana in middle of the age followed by panchakarma, adopting pratimarsha nasya, doompana, gandoosha and Anjana as din charya administration of medication in early stage of disease are helpfull in delaying or arresting senile ocular condition.


2000 ◽  
Vol 45 (2) ◽  
pp. 115-134 ◽  
Author(s):  
Stephen Beatty ◽  
Hui-Hiang Koh ◽  
M Phil ◽  
David Henson ◽  
Michael Boulton

2016 ◽  
Vol 2016 ◽  
pp. 1-12 ◽  
Author(s):  
Janusz Blasiak ◽  
Russel J. Reiter ◽  
Kai Kaarniranta

Melatonin, an indoleamine, is synthesized mainly in the pineal gland in a circadian fashion, but it is produced in many other organs, including the retina, which seems to be especially important as the eye is a primary recipient of circadian signals. Melatonin displays strong antioxidative properties, which predispose it to play a protective role in many human pathologies associated with oxidative stress, including premature aging and degenerative disease. Therefore, melatonin may play a role in age-related macular degeneration (AMD), a disease affecting photoreceptors, and retinal pigment epithelium (RPE) with an established role of oxidative stress in its pathogenesis. Several studies have shown that melatonin could exert the protective effect against damage to RPE cells evoked by reactive oxygen species (ROS), but it has also been reported to increase ROS-induced damage to photoreceptors and RPE. Melatonin behaves like synthetic mitochondria-targeted antioxidants, which concentrate in mitochondria at relatively high levels; thus, melatonin may prevent mitochondrial damage in AMD. The retina contains telomerase, an enzyme implicated in maintaining the length of telomeres, and oxidative stress inhibits telomere synthesis, while melatonin overcomes this effect. These features support considering melatonin as a preventive and therapeutic agent in the treatment of AMD.


Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 790
Author(s):  
Ravirajsinh Jadeja ◽  
Pamela Martin

Inflammation and oxidative stress play prominent roles in the pathogenesis of many degenerative diseases of the retina, such as age-related macular degeneration (AMD), diabetic retinopathy (DR), retinal vein occlusion, and retinitis pigmentosa [1–3]. [...]


2019 ◽  
Vol 24 (40) ◽  
pp. 4726-4741 ◽  
Author(s):  
Orathai Tangvarasittichai ◽  
Surapon Tangvarasittichai

Background: Oxidative stress is caused by free radicals or oxidant productions, including lipid peroxidation, protein modification, DNA damage and apoptosis or cell death and results in cellular degeneration and neurodegeneration from damage to macromolecules. Results: Accumulation of the DNA damage (8HOdG) products and the end products of LPO (including aldehyde, diene, triene conjugates and Schiff’s bases) were noted in the research studies. Significantly higher levels of these products in comparison with the controls were observed. Oxidative stress induced changes to ocular cells and tissues. Typical changes include ECM accumulation, cell dysfunction, cell death, advanced senescence, disarrangement or rearrangement of the cytoskeleton and released inflammatory cytokines. It is involved in ocular diseases, including keratoconus, Fuchs endothelial corneal dystrophy, and granular corneal dystrophy type 2, cataract, age-related macular degeneration, primary open-angle glaucoma, retinal light damage, and retinopathy of prematurity. These ocular diseases are the cause of irreversible blindness worldwide. Conclusions: Oxidative stress, inflammation and autophagy are implicated in biochemical and morphological changes in these ocular tissues. The development of therapy is a major target for the management care of these ocular diseases.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Donita L. Garland ◽  
Eric A. Pierce ◽  
Rosario Fernandez-Godino

AbstractThe complement system plays a role in the formation of sub-retinal pigment epithelial (RPE) deposits in early stages of age-related macular degeneration (AMD). But the specific mechanisms that connect complement activation and deposit formation in AMD patients are unknown, which limits the development of efficient therapies to reduce or stop disease progression. We have previously demonstrated that C3 blockage prevents the formation of sub-RPE deposits in a mouse model of EFEMP1-associated macular degeneration. In this study, we have used double mutant Efemp1R345W/R345W:C5-/- mice to investigate the role of C5 in the formation of sub-RPE deposits in vivo and in vitro. The data revealed that the genetic ablation of C5 does not eliminate the formation of sub-RPE deposits. Contrarily, the absence of C5 in RPE cultures promotes complement dysregulation that results in increased activation of C3, which likely contributes to deposit formation even in the absence of EFEMP1-R345W mutant protein. The results also suggest that genetic ablation of C5 alters the extracellular matrix turnover through an effect on matrix metalloproteinases in RPE cell cultures. These results confirm that C3 rather than C5 could be an effective therapeutic target to treat early AMD.


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