Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2022 Oct 22:2022:9800838.
doi: 10.1155/2022/9800838. eCollection 2022.

View of the Renin-Angiotensin System in Acute Kidney Injury Induced by Renal Ischemia-Reperfusion Injury

Farzaneh Karimi  1 , Maryam Maleki  2 , Mehdi Nematbakhsh  3
Affiliations
Review

View of the Renin-Angiotensin System in Acute Kidney Injury Induced by Renal Ischemia-Reperfusion Injury

Farzaneh Karimi et al. J Renin Angiotensin Aldosterone Syst. .

Abstract

Renal ischemia-reperfusion injury (RIRI) is a sequence of complicated events that is defined as a reduction of the blood supply followed by reperfusion. RIRI is the leading cause of acute kidney injury (AKI). Among the diverse mediators that take part in RIRI-induced AKI, the renin-angiotensin system (RAS) plays an important role via conventional (angiotensinogen, renin, angiotensin-converting enzyme (ACE), angiotensin (Ang) II, and Ang II type 1 receptor (AT1R)) and nonconventional (ACE2, Ang 1-7, Ang 1-9, AT2 receptor (AT2R), and Mas receptor (MasR)) axes. RIRI alters the balance of both axes so that RAS can affect RIRI-induced AKI. In overall, the alteration of Ang II/AT1R and AKI by RIRI is important to consider. This review has looked for the effects and interactions of RAS activities during RIRI conditions.

PubMed Disclaimer

Conflict of interest statement

The authors declare no conflict of interest.

Similar articles

See all similar articles

Cited by

References

    1. Karimi F., Nematbakhsh M. Mas receptor blockade promotes renal vascular response to Ang II after partial kidney ischemia/reperfusion in a two-kidney-one-clip hypertensive rats model. International Journal of Nephrology . 2021;2021:8. doi: 10.1155/2021/6618061.6618061 - DOI - PMC - PubMed
    1. Bonventre J. V., Zuk A. Ischemic acute renal failure: an inflammatory disease? Kidney International . 2004;66(2):480–485. doi: 10.1111/j.1523-1755.2004.761_2.x. - DOI - PubMed
    1. Legrand M., Mik E. G., Johannes T., Payen D., Ince C. Renal hypoxia and dysoxia after reperfusion of the ischemic kidney. Molecular Medicine . 2008;14(7-8):502–516. doi: 10.2119/2008-00006.Legrand. - DOI - PMC - PubMed
    1. Makris K., Spanou L. Acute kidney injury: definition, pathophysiology and clinical phenotypes. The Clinical Biochemist Reviews . 2016;37(2):85–98. - PMC - PubMed
    1. Schrier R. W., Wang W., Poole B., Mitra A. Acute renal failure: definitions, diagnosis, pathogenesis, and therapy. The Journal of Clinical Investigation . 2004;114(1):5–14. doi: 10.1172/JCI200422353. - DOI - PMC - PubMed

LinkOut - more resources