Abstract
Oxidative stress (OS) is an imbalance between free radicals/ROS and antioxidants, which evokes a biological response and is an important risk factor for diseases, in both the cardiovascular system and central nervous system (CNS). The underlying mechanisms driving pathophysiological complications that arise from OS remain largely unclear. The vascular endothelium is emerging as a primary target of excessive glucocorticoid and catecholamine action. Endothelial dysfunction (ED) has been implicated to play a crucial role in the development of neurodegeneration in the CNS. The retina is known as an extension of the CNS. Stress and endothelium dysfunction are suspected to be interlinked and associated with neurodegenerative diseases in the retina as well. In this narrative review, we explore the role of OS-led ED in the retina by focusing on mechanistic links between OS and ED, ED in the pathophysiology of different retinal neurodegenerative conditions, and how a better understanding of the role of endothelial function could lead to new therapeutic approaches for neurodegenerative diseases in the retina.
Highlights
Oxidative stress (OS) may contribute to subsequent oxidative modifications or damage to lipids, proteins, and DNA, with deleterious consequences for metabolism and cardiovascular disease [9], which is considered to be responsible for the pathogenesis of numerous age-related neurodegenerative diseases
The results of a systematic review and metaanalysis of randomized controlled trials indicated that markers of oxidative stress were increased in glaucoma overall, which ranged from an effect size of 1.29 in serum to 2.62 in aqueous humor
La Favor et al [82] exploited a novel microdialysis technique that allows simultaneous measurement of Reactive oxygen species (ROS) levels and microvascular endothelial function in vivo. They discovered that elevated levels of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-derived ROS in obese subjects were associated with microvascular Endothelial dysfunction (ED), such as impaired acetylcholine-induced increases in blood flow
Summary
Publisher’s Note: MDPI stays neutral with regard to jurisdictional claims in published maps and institutional affiliations. The results of a systematic review and metaanalysis of randomized controlled trials indicated that markers of oxidative stress were increased in glaucoma overall Antioxidative stress markers in serum were decreased The increase in some antioxidant markers is probably a protective response of the eye to oxidative stress [16]. Special receptors on EC membranes initiate intracellular signal cascades in response to agonists that activate specific receptors or changes in cell surface shear stress caused by changes in blood flow rate. Gap junctions allow crosstalk between adjacent ECs, thereby allowing the transmission of intracellular reactions Once activated, these cascades trigger the release of potent vasodilator substances, such as nitric oxide (NO) and prostaglandins and vasoconstrictors, such as endothelin and endothelium-derived vasoconstrictors [25–27]. This review focuses on the impact of OS on endothelial function and the roles of endothelial dysfunction (ED) in retinal neurodegenerative diseases
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