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. 2023 Jul 28;37(4):268-280.
doi: 10.7555/JBR.36.20220261.

Do reactive oxygen species damage or protect the heart in ischemia and reperfusion? Analysis on experimental and clinical data

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Do reactive oxygen species damage or protect the heart in ischemia and reperfusion? Analysis on experimental and clinical data

Leonid N Maslov et al. J Biomed Res. .

Abstract

The role of reactive oxygen species (ROS) in ischemic and reperfusion (I/R) injury of the heart has been discussed for more than 40 years. It has been demonstrated that reperfusion triggers a multiple increase in free radical generation in the isolated heart. Antioxidants were found to have the ability to mitigate I/R injury of the heart. However, it is unclear whether their cardioprotective effect truly depends on the decrease of ROS levels in myocardial tissues. Since high doses and high concentrations of antioxidants were experimentally used, it is highly likely that the cardioprotective effect of antioxidants depends on their interaction not only with free radicals but also with other molecules. It has been demonstrated that the antioxidant N-2-mercaptopropionyl glycine or NDPH oxidase knockout abolished the cardioprotective effect of ischemic preconditioning. Consequently, there is evidence that ROS protect the heart against the I/R injury.

Keywords: antioxidants; free radicals; heart; patients; reactive oxygen species; reperfusion.

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Conflict of interest statement

The authors reported no conflict of interests.

Figures

Figure 1
Figure 1
The antioxidants-triggered cardioprotection.
Figure 2
Figure 2
Signaling mechanism of reactive oxygen species triggering cardioprotection.

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References

    1. Bilenko MV. Ischemic and reperfusion injury to organs[M]. Moscow: Meditsina, 1989: 368.

    1. Meerson FZ. Pathogenesis and prevention of stress and ischemic injuries of the heart[M]. Moscow: Meditsina, 1984: 272.

    1. Meerson FZ, Krasikov SI, Ustinova EE, et al Prevention of heart damage by extreme physical stress and increasing its resistance to acute overstrain with the antioxidant ionol. https://europepmc.org/article/MED/3712957 Kardiologiia. 1986;26(4):70–74. - PubMed
    1. Yellon DM, Downey JM Preconditioning the myocardium: from cellular physiology to clinical cardiology. Physiol Rev. 2003;83(4):1113–1151. doi: 10.1152/physrev.00009.2003. - DOI - PubMed
    1. Krylatov AV, Maslov LN, Voronkov NS, et al Reactive oxygen species as intracellular signaling molecules in the cardiovascular system. Curr Cardiol Rev. 2018;14(4):290–300. doi: 10.2174/1573403X14666180702152436. - DOI - PMC - PubMed