Cited by 618Cardiac Ischemia and ReperfusionMitochondrial Function and PathologyNeuroprotection in Cerebral Ischemia

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Targeting an antioxidant to mitochondria decreases cardiac ischemia-reperfusion injury

Adlam, Victoria J., Harrison, Joanne C., Porteous, Carolyn M., James, Andrew M., Smith, Robin A. J., Murphy, Michael P., Sammut, Ivan A.·2005·The FASEB Journal

DOI 10.1096/fj.05-3718com

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Abstract

Mitochondrial oxidative damage contributes to a wide range of pathologies, including cardiovascular disorders and neurodegenerative diseases. Therefore, protecting mitochondria from oxidative damage should be an effective therapeutic strategy. However, conventional antioxidants have limited efficacy due to the difficulty of delivering them to mitochondria in situ. To overcome this problem, we developed mitochondria‐targeted antioxidants, typified by MitoQ, which comprises a lipophilic triphenylphosphonium (TPP) cation covalently attached to a ubiquinol antioxidant. Driven by the large mitochondrial membrane potential, the TPP cation concentrates MitoQ several hundred‐fold within mitochondria, selectively preventing mitochondrial oxidative damage. To test whether MitoQ was active in vivo, we chose a clinically relevant form of mitochondrial oxidative damage: cardiac ischemia‐reperfusion injury. Feeding MitoQ to rats significantly decreased heart dysfunction, cell death, and mitochondrial damage after ischemia‐reperfusion. This protection was due to the antioxidant activity of MitoQ within mitochondria, as an untargeted antioxidant was ineffective and accumulation of the TPP cation alone gave no protection. Therefore, targeting antioxidants to mitochondria in vivo is a promising new therapeutic strategy in the wide range of human diseases such as Parkinson's disease, diabetes, and Friedreich's ataxia where mitochondrial oxidative damage underlies the pathology. Adlam, V. J., Harrison, J. C., Porteous, C. M., James, A. M., Smith, R. A. J., Murphy, M. P., Sammut, I. A. Targeting an antioxidant to mitochondria decreases cardiac ischemia‐reperfusion injury. FASEB J. 19, 1088–1095 (2005)

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Authors: Adlam, V. J., Harrison, J. C., Porteous, C. M., James, A. M., Smith, R. A. J., Murphy, M. P., & Sammut, I. A.
Affiliations: University of Otago (NZ)
MRC Mitochondrial Biology Unit (GB)
ORCID: Harrison, Joanne C.
James, Andrew M.
Murphy, Michael P.
Sammut, Ivan A.
Venue: The FASEB Journal
Publisher: Wiley
Published: 2005-07
Volume: 19
Issue: 9
Pages: 1088-1095
ISSN: 0892-6638 (ISSN-L)
1530-6860
DOI: 10.1096/fj.05-3718com
OpenAlex: W2060179384
Semantic Scholar: 7c4097d1a1a2771b393d479d8b5d4e5cf4eeeacb
Cited by: 618
References: 39
Citations by year: 2026: 10 · 2025: 26 · 2024: 11 · 2023: 17 · 2022: 28 · 2021: 28 · 2020: 38 · 2019: 36 · 2018: 32 · 2017: 25 · 2016: 32 · 2015: 40 · 2014: 45 · 2013: 33 · 2012: 34
FWCI: 19.15
Type: journal article
Language: en
Open access: closed
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: The FASEB Journal (publishedVersion)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Life Sciences › Neuroscience › Neurology › Neuroprotection in Cerebral Ischemia
Keywords: mitochondria-targeted antioxidants, MitoQ, myocardial ischemia-reperfusion injury, mitochondrial oxidative damage, triphenylphosphonium cation, ubiquinol, mitochondrial membrane potential, cardiac dysfunction, mitochondrial cell death, Parkinson's disease, Friedreich's ataxia, diabetes mellitus
MeSH terms: Animals, Antioxidants, Heart, Male, Mitochondria, Organophosphorus Compounds, Oxygen Consumption, Ubiquinone, Myocardial Reperfusion Injury, Rats, Wistar, Protective Agents, Cytochromes c, Rats

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Targeting an antioxidant to mitochondria decreases cardiac ischemia-reperfusion injury

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