ArticlePloS one2009
Ectopic catalase expression in mitochondria by adeno-associated virus enhances exercise performance in mice.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Spermidine toxicity in Saccharomyces cerevisiae due to mitochondrial complex III deficiency.Biogerontology · 2025Article
- Exercise performance in well-trained male mice is promoted by intermittent hyperoxia via improving metabolic properties and capillary profiles.Physiological reports · 2025Article
- Exercise and mitochondrial mechanisms in patients with sarcopenia.Frontiers in physiology · 2022Review
- Metabolic derangement in polycystic kidney disease mouse models is ameliorated by mitochondrial-targeted antioxidants.Communications biology · 2021Article
- Late-life restoration of mitochondrial function reverses cardiac dysfunction in old mice.eLife · 2020Article
- Fatiguing contractions increase protein S-glutathionylation occupancy in mouse skeletal muscle.Redox biology · 2018Article
- Mitochondria in the middle: exercise preconditioning protection of striated muscle.The Journal of physiology · 2016Review
- Peroxisome-mitochondria interplay and disease.Journal of inherited metabolic disease · 2015Review
- Genetically enhancing mitochondrial antioxidant activity improves muscle function in aging.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- The mitochondrial unfolded protein response and increased longevity: cause, consequence, or correlation?Experimental gerontology · 2014Review
- Mitochondrial oxidative stress in aging and healthspan.Longevity & healthspan · 2014Review
- Mitochondrial-targeted peptide rapidly improves mitochondrial energetics and skeletal muscle performance in aged mice.Aging cell · 2013Article
- Mitochondria-targeted antiaging gene therapy with adeno-associated viral vectors.Methods in molecular biology (Clifton, N.J.) · 2013Article
- Novel therapies targeting inner mitochondrial membrane--from discovery to clinical development.Pharmaceutical research · 2011Review
- The importance of mitochondrial DNA in aging and cancer.Journal of aging research · 2011Article
- Article
- Monitoring murine skeletal muscle function for muscle gene therapy.Methods in molecular biology (Clifton, N.J.) · 2011Article
- Mitochondrial oxidative stress and mammalian healthspan.Mechanisms of ageing and developmentReview
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Oxidative stress is thought to compromise muscle contractility. However, administration of generic antioxidants has failed to convincingly improve performance during exhaustive exercise. One possible explanation may relate to the inability of the supplemented antioxidants to effectively eliminate excessive free radicals at the site of generation. Here, we tested whether delivering catalase to the mitochondria, a site of free radical production in contracting muscle, could improve treadmill performance in C57Bl/6 mice. Recombinant adeno-associated virus serotype-9 (AV.RSV.MCAT) was generated to express a mitochondria-targeted catalase gene. AV.RSV.MCAT was delivered to newborn C57Bl/6 mouse circulation at the dose of 10(12) vector genome particles per mouse. Three months later, we observed a approximately 2 to 10-fold increase of catalase protein and activity in skeletal muscle and the heart. Subcellular fractionation western blot and double immunofluorescence staining confirmed ectopic catalase expression in the mitochondria. Compared with untreated control mice, absolute running distance and body weight normalized running distance were significantly improved in AV.RSV.MCAT infected mice during exhaustive treadmill running. Interestingly, ex vivo contractility of the extensor digitorum longus muscle was not altered. Taken together, we have demonstrated that forced catalase expression in the mitochondria enhances exercise performance. Our result provides a framework for further elucidating the underlying mechanism. It also raises the hope of applying similar strategies to remove excessive, pathogenic free radicals in certain muscle diseases (such as Duchenne muscular dystrophy) and ameliorate muscle disease.
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Registered trials
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