Targeting an antioxidant to mitochondria decreases cardiac ischemia‐reperfusion injury

By Victoria J Adlam, J. C. Harrison, C. M. Porteous, A. James, Robin A. J. Smith, M. Murphy, I. Sammut. The FASEB Journal, 2005

611 citations recorded by the source corpus.

Subfields: Biophysics, Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/7c4097d1a1a2771b393d479d8b5d4e5cf4eeeacb

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Biophysics

1. M. Jackson
2. S. Powers
3. M. Yorek
4. W. Sivitz

In Molecular Biology

1. Guido Kroemer
2. L. Galluzzi
3. C. Brenner
4. W. Gu
5. M. Jackson
6. S. Powers
7. E. Murphy
8. M. Yorek

In Pathology and Forensic Medicine

1. Guido Kroemer
2. E. Murphy
3. C. Steenbergen

Citations in the corpus

• Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury. (2008, background): “provide some reduction in infarct size (1, 27, 228).”
• Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010, positive): “Oral administration of mitoQ (500 m M in drinking water administered ad libitum ) to normal male rats protected heart muscle function, prevented myocardial cell death, and improved the respiratory-control ratio (state 3 to state 4 respiration) in rats subject to ischemia = reperfusion injury (7).”
• Exercise-Induced Oxidative Stress: Cellular Mechanisms and Impact on Muscle Force Production (2008, background): “For example, using a mitochondrial targeted antioxidant, researchers could study specific mitochondrial ROS production and its consequences using organelle specific antioxidants (5, 57, 274, 369).”
• Glutathione Peroxidase-1 in Health and Disease: From Molecular Mechanisms to Therapeutic Opportunities (2011, neutral): “…is consistent with the effects of antioxidants, such as N-acetyl-L-cysteine; MitoQ, a mitochondrially targeted antioxidant lipophilic tri-phenylphosphonium cation covalently bound to a ubiquinol antioxidant (2); and diphenylene iodonium, an inhibitor of NOX, in attenuating ROS-induced apoptosis.”
• Mitochondrial membrane permeabilization in cell death. (2007, background): “Recently, MitoQ, an ubiquinol antioxidant coupled to a mitochondrion-targeting lipophilic cation, has been shown to efficiently protect rats from mitochondrial damage, cell death, and cardiac dysfunction upon ischemia/ reperfusion injury (4).”
• Ferroptosis as a target for protection against cardiomyopathy (2019, result): “This is consistent with a previous report that MitoQ, a mitochondria-targeted antioxidant, significantly reduced cardiac I/R-related heart dysfunction, cell death, and mitochondrial damage, whereas an untargeted antioxidant did not confer cardioprotection (46).”