Antioxidants and neurodegenerative eye disease

Semenova, Yuliya; Bjørklund, Geir

doi:10.1080/10408398.2023.2215865

Cited by 4 publications

(5 citation statements)

References 130 publications

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“…Indeed, one pivotal element in the pathophysiology of neurodegenerative eye disease such as AMD is certainly oxidative stress [ 6 ] ( Figure 1 ).…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, neuroinflammation and ocular ischemia also have a significant impact on the disease. Antioxidants, either by food or oral supplementation, may be able to mitigate the deleterious effects of reactive oxygen species (ROS) that build because of oxidative stress, ischemia, and inflammation by reducing the expression of the genes involved in retinal inflammation [ 6 ].…”

Section: Introductionmentioning

confidence: 99%

“…In 2001, the Age-Related Eye Disease Study (AREDS) [4] first showed that patients with advanced AMD, or those with at least intermediate AMD (defined as bilateral large drusen with or without pigment changes) [5], could benefit from taking oral antioxidant vitamin and mineral supplements [4]. Indeed, one pivotal element in the pathophysiology of neurodegenerative eye disease such as AMD is certainly oxidative stress [6] (Figure 1). Indeed, one pivotal element in the pathophysiology of neurodegenerative eye disease such as AMD is certainly oxidative stress [6] (Figure 1).…”

Section: Introductionmentioning

confidence: 99%

“…Indeed, one pivotal element in the pathophysiology of neurodegenerative eye disease such as AMD is certainly oxidative stress [6] (Figure 1). Indeed, one pivotal element in the pathophysiology of neurodegenerative eye disease such as AMD is certainly oxidative stress [6] (Figure 1). In response to oxidative stress, which can be induced by molecules like lipopolysaccharides, exosomes derived from retinal pigment epithelial cells (RPE) can induce inflammation in the retina and thus contribute to AMD pathogenesis.…”

Section: Introductionmentioning

confidence: 99%

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The Role of Oral Supplementation for the Management of Age-Related Macular Degeneration: A Narrative Review

D’Angelo,

Vitiello,

Gagliardi

et al. 2024

JPM

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The majority of neurodegenerative eye disorders occur with aging and significantly impair quality of life. Age-related macular degeneration (AMD) is the third most common cause of visual impairment and blindness worldwide. One of the most important elements in the pathophysiology of neurodegenerative eye disease is certainly oxidative stress, with neuroinflammation and ocular ischemia which may also be significant factors. Antioxidants, either by food or oral supplementation, may be able to mitigate the deleterious effects of reactive oxygen species that build as a result of oxidative stress, ischemia, and inflammation. Over the past few decades, a number of research works examining the potential adjuvant impact of antioxidants in AMD have been published. In fact, there is not only more and more interest in already known molecules but also in new molecules that can help clinicians in the management of this complex multifactorial disease, such as astaxanthin and melatonin. However, while some studies showed encouraging outcomes, others were conflicting. In addition, more and more attention is also being paid to nutrition, considered a pivotal key point, especially to prevent AMD. For this reason, the purpose of this review is to analyze the main antioxidant molecules currently used as oral supplements for AMD treatment, as well as the role of diet and food intake in this ocular disease, to better understand how all these factors can improve the clinical management of AMD patients.

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“…Indeed, one pivotal element in the pathophysiology of neurodegenerative eye disease such as AMD is certainly oxidative stress [ 6 ] ( Figure 1 ).…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

The Role of Oral Supplementation for the Management of Age-Related Macular Degeneration: A Narrative Review

D’Angelo,

Vitiello,

Gagliardi

et al. 2024

JPM

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“…Oxidative stress has been implicated in the pathogenesis of glaucoma, a group of diseases characterized by the progressive loss of RGCs and their axons, resulting in optic nerve head excavation and visual field defects. Oxidative stress can affect various ocular tissues, such as the TM, retina, and optic nerve head while contributing to increased IOP, neuroinflammation, and apoptosis [26][27][28]. These findings suggest that oxidative stress may play a key role in glaucoma pathophysiology and may represent a potential target for novel therapeutic interventions.…”

Section: Introductionmentioning

confidence: 99%

scAAV2-Mediated Expression of Thioredoxin 2 and C3 Transferase Prevents Retinal Ganglion Cell Death and Lowers Intraocular Pressure in a Mouse Model of Glaucoma

Kim,

Cha,

Choi

et al. 2023

IJMS

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Elevated intraocular pressure (IOP) in glaucoma causes retinal ganglion cell (RGC) loss and damage to the optic nerve. Although IOP is controlled pharmacologically, no treatment is available to restore retinal and optic nerve function. In this paper, we aimed to develop a novel gene therapy for glaucoma using an AAV2-based thioredoxin 2 (Trx2)-exoenzyme C3 transferase (C3) fusion protein expression vector (scAAV2-Trx2-C3). We evaluated the therapeutic effects of this vector in vitro and in vivo using dexamethasone (DEX)-induced glaucoma models. We found that scAAV2-Trx2-C3-treated HeLa cells had significantly reduced GTP-bound active RhoA and increased phosphor-cofilin Ser3 protein expression levels. scAAV2-Trx2-C3 was also shown to inhibit oxidative stress, fibronectin expression, and alpha-SMA expression in DEX-treated HeLa cells. NeuN immunostaining and TUNEL assay in mouse retinal tissues was performed to evaluate its neuroprotective effect upon RGCs, whereas changes in mouse IOP were monitored via rebound tonometer. The present study showed that scAAV2-Trx2-C3 can protect RGCs from degeneration and reduce IOP in a DEX-induced mouse model of glaucoma, while immunohistochemistry revealed that the expression of fibronectin and alpha-SMA was decreased after the transduction of scAAV2-Trx2-C3 in murine eye tissues. Our results suggest that AAV2-Trx2-C3 modulates the outflow resistance of the trabecular meshwork, protects retinal and other ocular tissues from oxidative damage, and may lead to the development of a gene therapeutic for glaucoma.

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