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Review
. 2015 Nov 20;16(11):27770-80.
doi: 10.3390/ijms161126059.

Redox Roles of Reactive Oxygen Species in Cardiovascular Diseases

Affiliations
Review

Redox Roles of Reactive Oxygen Species in Cardiovascular Diseases

Feng He et al. Int J Mol Sci. .

Abstract

Cardiovascular disease (CVD), a major cause of mortality in the world, has been extensively studied over the past decade. However, the exact mechanism underlying its pathogenesis has not been fully elucidated. Reactive oxygen species (ROS) play a pivotal role in the progression of CVD. Particularly, ROS are commonly engaged in developing typical characteristics of atherosclerosis, one of the dominant CVDs. This review will discuss the involvement of ROS in atherosclerosis, specifically their effect on inflammation, disturbed blood flow and arterial wall remodeling. Pharmacological interventions target ROS in order to alleviate oxidative stress and CVD symptoms, yet results are varied due to the paradoxical role of ROS in CVD. Lack of effectiveness in clinical trials suggests that understanding the exact role of ROS in the pathophysiology of CVD and developing novel treatments, such as antioxidant gene therapy and nanotechnology-related antioxidant delivery, could provide a therapeutic advance in treating CVDs. While genetic therapies focusing on specific antioxidant expression seem promising in CVD treatments, multiple technological challenges exist precluding its immediate clinical applications.

Keywords: antioxidant; atherosclerosis; free radical; reactive oxygen species.

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References

    1. Fearon I.M., Faux S.P. Oxidative stress and cardiovascular disease: Novel tools give (free) radical insight. J. Mol. Cell. Cardiol. 2009;47:372–381. doi: 10.1016/j.yjmcc.2009.05.013. - DOI - PubMed
    1. Mozaffarian D., Benjamin E.J., Go A.S., Arnett D.K., Blaha M.J., Cushman M., de Ferranti S., Despres J.P., Fullerton H.J., Howard V.J., et al. Heart disease and stroke statistics—2015 update: A report from the american heart association. Circulation. 2015;131:e29–e322. doi: 10.1161/CIR.0000000000000152. - DOI - PubMed
    1. Ross R. The pathogenesis of atherosclerosis: A perspective for the 1990s. Nature. 1993;362:801–809. doi: 10.1038/362801a0. - DOI - PubMed
    1. Frostegard J. Immunity, atherosclerosis and cardiovascular disease. BMC Med. 2013;11 doi: 10.1186/1741-7015-11-117. - DOI - PMC - PubMed
    1. Rader D.J., Daugherty A. Translating molecular discoveries into new therapies for atherosclerosis. Nature. 2008;451:904–913. doi: 10.1038/nature06796. - DOI - PubMed

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