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Review
. 2022 Apr 4:2022:7906091.
doi: 10.1155/2022/7906091. eCollection 2022.

Reactive Oxygen Species and Oxidative Stress in Vascular-Related Diseases

Xin-Meng Cheng  1 , Yu-Yuan Hu  1 , Tao Yang  1 , Nan Wu  1 , Xue-Ning Wang  1
Affiliations
Review

Reactive Oxygen Species and Oxidative Stress in Vascular-Related Diseases

Xin-Meng Cheng et al. Oxid Med Cell Longev. .

Abstract

Oxidative stress (OS) refers to the enhancement of oxidation and the decreased of related antioxidant enzymes activity under pathological conditions, resulting in relatively excess reactive oxygen species (ROS), causing cytotoxicity, which leads to tissue damage and is linked to neurodegenerative diseases, cardiovascular diseases, diabetes, cancers, and many other pathologies. As an important intracellular signaling molecule, ROS can regulate numerous physiological actions, such as vascular reactivity and neuronal function. According to several studies, the uncontrolled production of ROS is related to vascular injury. The growing evidence revealing how traditional risk factors translate into ROS and lead to vasculitis and other vascular diseases. In this review, we sought to mainly discuss the role of ROS and antioxidant mechanisms in vascular-related diseases, especially cardiovascular and common macrovascular diseases.

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Conflict of interest statement

The authors declare that they have no competing interests.

Figures

Figure 1
Figure 1
Sources of ROS production. (a) ROS from the NOX2. (b) Electron transfer and ROS generation in ETC. (c) Uncoupled eNOS produced superoxide. (d) OX produced superoxide and hydrogen peroxide by degrading of purines and conversion of hypoxanthine.
Figure 2
Figure 2
The related mechanism of ROS and diseases.
See this image and copyright information in PMC

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References

    1. Halliwell B. The role of oxygen radicals in human disease, with particular reference to the vascular system. Haemostasis . 1993;23(Supplement 1):118–126. - PubMed
    1. Kaludercic N., Di Lisa F. Mitochondrial ROS formation in the pathogenesis of diabetic cardiomyopathy. Frontiers in Cardiovascular Medicine . 2020;7:p. 12. doi: 10.3389/fcvm.2020.00012. - DOI - PMC - PubMed
    1. Kattoor A. J., Pothineni N. V. K., Palagiri D., Mehta J. L. Oxidative stress in atherosclerosis. Current Atherosclerosis Reports . 2017;19(11):p. 42. doi: 10.1007/s11883-017-0678-6. - DOI - PubMed
    1. Ruan Y., Jiang S., Musayeva A., Gericke A. Oxidative stress and vascular dysfunction in the retina: therapeutic strategies. Antioxidants . 2020;9(8) doi: 10.3390/antiox9080761. - DOI - PMC - PubMed
    1. Thomas S. R., Witting P. K., Drummond G. R. Redox control of endothelial function and dysfunction: molecular mechanisms and therapeutic opportunities. Antioxidants & Redox Signaling . 2008;10(10):1713–1766. doi: 10.1089/ars.2008.2027. - DOI - PubMed