Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Journal Club
  • Published:

Metabolism

Uncovering the origin of oxidative damage in ischaemia–reperfusion injury in the heart

Nature Reviews Endocrinology volume 19, page 560 (2023)Cite this article

Subjects

Heart disease is currently considered the leading cause of death worldwide, and coronary artery disease — the most common type of heart disease — underlies most cases of myocardial infarction. Myocardial infarction arises from the rupture of an atherosclerotic plaque, which causes the formation of a clot and occludes the blood supply in large epicardial coronary arteries. This disrupted blood flow and consequent decrease in the supply of oxygen is known as ischaemia.

Reperfusion therapy, usually through thrombolytic agents, is essential for cell and organ survival, but the mere act of restoring the blood supply after a period of ischaemia is known to induce cellular injury itself. This paradoxical outcome is called ischaemia–reperfusion injury and can lead to the death of cardiomyocytes, increasing the infarct size by up to 50%. Of note, ischaemia–reperfusion injury not only occurs in the heart, but can also affect other key metabolic organs (such as the brain, liver and kidneys) when the blood supply is restored after ischaemia in these tissues.

This is a preview of subscription content, access via your institution

Access options

Buy this article

  • Purchase on Springer Link
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

References

Original article

Related articles

  • Zweier, J. L. Measurement of superoxide-derived free radicals in the reperfused heart. J. Biol. Chem. 263, 1353–1357 (1988)

    Article  CAS  PubMed  Google Scholar 

  • Valls-Lacalle, L. et al. Selective inhibition of succinate dehydrogenase in reperfused myocardium with intracoronary malonate reduces infarct size. Sci. Rep. 8, 2442 (2018)

    Article  PubMed  PubMed Central  Google Scholar 

  • Jespersen, N. R. et al. Cardioprotective effect of succinate dehydrogenase inhibition in rat hearts and human myocardium with and without diabetes mellitus. Sci. Rep. 10, 10344 (2020)

    Article  CAS  PubMed  PubMed Central  Google Scholar 

Download references

Author information

Authors and Affiliations

  1. Wellcome–MRC Institute of Metabolic Science and Medical Research Council Metabolic Diseases Unit, University of Cambridge, Cambridge, UK

    Elizabeth Figueroa-Juárez

Authors
  1. Elizabeth Figueroa-Juárez
    View author publications

    You can also search for this author in PubMed Google Scholar

Corresponding author

Correspondence to Elizabeth Figueroa-Juárez.

Ethics declarations

Competing interests

The author declares no competing interests.

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Figueroa-Juárez, E. Uncovering the origin of oxidative damage in ischaemia–reperfusion injury in the heart. Nat Rev Endocrinol 19, 560 (2023). https://doi.org/10.1038/s41574-023-00881-w

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/s41574-023-00881-w

Search

Advanced search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing