Protection against renal ischemia–reperfusion injury in vivo by the mitochondria targeted antioxidant MitoQ
Open accessAbstract
Ischemia-reperfusion (IR) injury to the kidney occurs in a range of clinically important scenarios including hypotension, sepsis and in surgical procedures such as cardiac bypass surgery and kidney transplantation, leading to acute kidney injury (AKI). Mitochondrial oxidative damage is a significant contributor to the early phases of IR injury and may initiate a damaging inflammatory response. Here we assessed whether the mitochondria targeted antioxidant MitoQ could decrease oxidative damage during IR injury and thereby protect kidney function. To do this we exposed kidneys in mice to in vivo ischemia by bilaterally occluding the renal vessels followed by reperfusion for up to 24h. This caused renal dysfunction, measured by decreased creatinine clearance, and increased markers of oxidative damage. Administering MitoQ to the mice intravenously 15 min prior to ischemia protected the kidney from damage and dysfunction. These data indicate that mitochondrial oxidative damage contributes to kidney IR injury and that mitochondria targeted antioxidants such as MitoQ are potential therapies for renal dysfunction due to IR injury.
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MitoQ has been shown to be protective against ischemia/reperfusion injury, cardiac hypertrophy, and hypertension in animal models.
“MitoQ has been used extensively in animal models of disease and been shown to be protective against ischemia/reperfusion injury, cardiac hypertrophy, and hypertension (210, 211) among other pathologies.”
From Sources of Vascular Nitric Oxide and Reactive Oxygen Species and Their Regulation (2019) · cites this paper as [210]
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- Authors
- Dare, A. J., Bolton, E. A., Pettigrew, G. J., Bradley, J. A., Saeb-Parsy, K., & Murphy, M. P.
- Affiliations
- MRC Mitochondrial Biology Unit (GB)
- University of Cambridge (GB)
- Corresponding author
- Murphy, Michael P.
- Venue
- Redox Biology
- Publisher
- Elsevier BV
- Published
- 2015-08
- Volume
- 5
- Pages
- 163-168
- ISSN
- 2213-2317 (ISSN-L)
- PMC
- PMC4427662
- OpenAlex
- W2074937649
- Cited by
- 202
- References
- 44
- Citations by year
- 2026: 10 · 2025: 22 · 2024: 11 · 2023: 17 · 2022: 18 · 2021: 25 · 2020: 26 · 2019: 20 · 2018: 17 · 2017: 11 · 2016: 16 · 2015: 7 · 2014: 1
- FWCI
- 14.73
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Redox Biology (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Medical Research Council
- NIHR Cambridge Biomedical Research Centre
- Topics
- Health Sciences › Medicine › Nephrology › Acute Kidney Injury Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Keywords
- renal ischemia-reperfusion injury, MitoQ, mitochondria-targeted antioxidants, mitochondrial oxidative damage, acute kidney injury, renal dysfunction, renal protection, renal ischemia, oxidative stress
- MeSH terms
- Animals, Antioxidants, Creatinine, Kidney, Male, Mice, Inbred C57BL, Mitochondria, Organophosphorus Compounds, Ubiquinone, Reperfusion Injury, Oxidative Stress, Mice
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