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Review
. 2022 Mar 12;11(3):543.
doi: 10.3390/antiox11030543.

Oxidative Stress, Vascular Endothelium, and the Pathology of Neurodegeneration in Retina

Affiliations
Review

Oxidative Stress, Vascular Endothelium, and the Pathology of Neurodegeneration in Retina

Xin Shi et al. Antioxidants (Basel). .

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.

Keywords: endothelium; neurodegeneration; oxidative stress; retina.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
NO and endothelium dysfunction.
Figure 2
Figure 2
Endothelium and neurodegenerative diseases in retina.

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References

    1. Chandrasekaran A., Idelchik M.D.P.S., Melendez J.A. Redox control of senescence and age-related disease. Redox Biol. 2017;11:91–102. doi: 10.1016/j.redox.2016.11.005. - DOI - PMC - PubMed
    1. Lobo V., Patil A., Phatak A., Chandra N. Free radicals, antioxidants and functional foods: Impact on human health. Pharmacogn. Rev. 2010;4:118–126. doi: 10.4103/0973-7847.70902. - DOI - PMC - PubMed
    1. Powers S.K., Ji L.L., Kavazis A.N., Jackson M.J. Reactive Oxygen Species: Impact on Skeletal Muscle. Compr. Physiol. 2011;1:941–969. doi: 10.1002/cphy.c100054. - DOI - PMC - PubMed
    1. Aikens J., Dix T.A. Perhydroxyl radical (HOO) initiated lipid peroxidation: The role of fatty acid hydroperoxides. J. Biol. Chem. 1991;266:15091–15098. doi: 10.1016/S0021-9258(18)98591-1. - DOI - PubMed
    1. Halliwell B., Gutteridge J.M. Free Radicals in Biology and Medicine. 3rd ed. Oxford University Press; Oxford, UK: 1999.

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