The DOI matches its Crossref record; 39 of the 39 references it cites were found in a registry or an index.
Targeting an antioxidant to mitochondria decreases cardiac ischemia-reperfusion injury
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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In the citing paper
“For example, Mitoquinone (MitoQ) has been tested successfully in human diseases such as Hepatitis C induced liver disease and skin photo damage as well as a number of experimental animal models including ischemia-reperfusion, neurodegenerative diseases, diabetes, and alcohol-induced hepatosteatosis [8–14].”
From Mitochondrially targeted compounds and their impact on cellular bioenergetics (2013) · cites this paper as [10]
In the citing paper
“A number of studies show that, when MitoQ is administered to in vivo animal models of pathologies, it reduces both oxidative damage and the pathologies (Adlam et al., 2005; Lowes et al., 2008; Graham et al., 2009; Supinski et al., 2009; Chacko et al., 2010; Smith and Murphy 2010).”
From The mitochondria-targeted antioxidant MitoQ prevents loss of spatial memory retention and early neuropathology in a transgenic mouse model of Alzheimer’s disease (2011) · cites this paper as Adlam et al., 2005
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Kelso, G. F., Porteous, C. M., Coulter, C. V., Hughes, G., Porteous, W. K., Ledgerwood, E. C., Smith, R. A. J., & Murphy, M. P. (2001) · Journal of Biological Chemistry · doi:10.1074/jbc.m009093200 · Cited by 1,091
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Delivery of bioactive molecules to mitochondria in vivo
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Kroemer, G., Galluzzi, L., & Brenner, C. (2007) · Physiological Reviews · doi:10.1152/physrev.00013.2006 · Cited by 3,598
Exercise-Induced Oxidative Stress: Cellular Mechanisms and Impact on Muscle Force Production
Powers, S. K., & Jackson, M. J. (2008) · Physiological Reviews · doi:10.1152/physrev.00031.2007 · Cited by 2,459
Ferroptosis as a target for protection against cardiomyopathy
Fang, X., Wang, H., Han, D., Xie, E., Yang, X., Wei, J., Gu, S., Gao, F., Zhu, N., Yin, X., et al. (2019) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1821022116 · Cited by 2,163
Bhatti, J. S., Bhatti, G. K., & Reddy, P. H. (2017) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2016.11.010 · Cited by 1,655
Mechanisms Underlying Acute Protection From Cardiac Ischemia-Reperfusion Injury
Murphy, E., & Steenbergen, C. (2008) · Physiological Reviews · doi:10.1152/physrev.00024.2007 · Cited by 1,504
Metadata
- 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)
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2005-07
- Volume
- 19
- Issue
- 9
- Pages
- 1088-1095
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- 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
- 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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