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.

  • News & Views
  • Published:

ACUTE KIDNEY INJURY

Nitric oxide protects against AKI by reprogramming metabolism

New findings demonstrate that endothelial nitric oxide synthase regulates major metabolic pathways in the kidney proximal tubule, which confers protection against oxidative stress during acute kidney injury (AKI). These findings give new insights into AKI pathophysiology and nitric oxide biology, and identify new targets for the treatment of AKI.

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

Access options

Buy this article

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

Fig. 1: Nitric oxide confers protection against AKI by shifting metabolic flux towards the pentose phosphate pathway.

References

  1. Zuk, A. & Bonventre, J. V. Acute kidney injury. Annu. Rev. Med. 67, 293–307 (2016).

    Article  CAS  Google Scholar 

  2. Zhou, H. L. et al. Metabolic reprogramming by the S-nitroso-CoA reductase system protects against kidney injury. Nature 565, 96–100 (2018).

    Article  Google Scholar 

  3. Lowenstein, C. J. & Snyder, S. H. Nitric oxide, a novel biologic messenger. Cell 70, 705–707 (1992).

    Article  CAS  Google Scholar 

  4. Stamler, J. S. et al. S-Nitrosylation of proteins with nitric oxide: synthesis and characterization of biologically active compounds. Proc. Natl Acad. Sci. USA 89, 444–448 (1992).

    Article  CAS  Google Scholar 

  5. Anand, P. et al. Identification of S-nitroso-CoA reductases that regulate protein S-nitrosylation. Proc. Natl Acad. Sci. USA 111, 18572–18577 (2014).

    Article  CAS  Google Scholar 

  6. Paynter, N. P. et al. Metabolic predictors of incident coronary heart disease in women. Circulation 137, 841–853 (2018).

    Article  Google Scholar 

  7. Qi, W. et al. Pyruvate kinase M2 activation may protect against the progression of diabetic glomerular pathology and mitochondrial dysfunction. Nat. Med. 23, 753–762 (2017).

    Article  CAS  Google Scholar 

  8. Ye, J. et al. Pyruvate kinase M2 promotes de novo serine synthesis to sustain mTORC1 activity and cell proliferation. Proc. Natl Acad. Sci. USA 109, 6904–6909 (2012).

    Article  CAS  Google Scholar 

  9. Katsyuba, E. et al. De novo NAD+ synthesis enhances mitochondrial function and improves health. Nature 563, 354–359 (2018).

    Article  CAS  Google Scholar 

  10. Poyan Mehr, A. et al. De novo NAD+ biosynthetic impairment in acute kidney injury in humans. Nat. Med. 24, 1351–1359 (2018).

    Article  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Pierre-Yves Martin.

Ethics declarations

Competing interests

The authors declare no competing interests.

Rights and permissions

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Martin, PY., de Seigneux, S. Nitric oxide protects against AKI by reprogramming metabolism. Nat Rev Nephrol 15, 195–196 (2019). https://doi.org/10.1038/s41581-019-0113-z

Download citation

  • Published:

  • Issue Date:

  • DOI: https://doi.org/10.1038/s41581-019-0113-z

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