ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2013
Mitochondria-targeted antioxidant promotes recovery of skeletal muscle mitochondrial function after burn trauma assessed by in vivo 31P nuclear magnetic resonance and electron paramagnetic resonance spectroscopy.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- Mitochondria as a Therapeutic Target for Burn Injury.Biomolecules · 2026Review
- Article
- Ferroptosis and mitochondrial dysfunction in acute central nervous system injury.Frontiers in cellular neuroscience · 2023Review
- SS-31 does not prevent or reduce muscle atrophy 7 days after a 65 kdyne contusion spinal cord injury in young male mice.Physiological reports · 2022Article
- A 50 kdyne contusion spinal cord injury with or without the drug SS-31 was not associated with major changes in muscle mass or gene expression 14 d after injury in young male mice.Physiological reports · 2021Article
- Protective Effect of Mitochondria-Targeted Antioxidants against Inflammatory Response to Lipopolysaccharide Challenge: A Review.Pharmaceutics · 2021Review
- The Genetic Evidence of Burn-Induced Cardiac Mitochondrial Metabolism Dysfunction.Biomedicines · 2020Article
- Improving mitochondrial function with SS-31 reverses age-related redox stress and improves exercise tolerance in aged mice.Free radical biology & medicine · 2019Article
- 2,4 Dinitrophenol as Medicine.Cells · 2019Review
- Abnormalities of Mitochondrial Dynamics in the Failing Heart: Normalization Following Long-Term Therapy with Elamipretide.Cardiovascular drugs and therapy · 2018Article
- The Role of Mitochondrial Stress in Muscle Wasting Following Severe Burn Trauma.Journal of burn care & research : official publication of the American Burn Association · 2018Review
- Rapid and simultaneous measurement of phosphorus metabolite pool size ratio and reaction kinetics of enzymes in vivo.Journal of magnetic resonance imaging : JMRI · 2018Article
- DNP, mitochondrial uncoupling, and neuroprotection: A little dab'll do ya.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2017Article
- Enzyme-Assisted Discovery of Antioxidant Peptides from Edible Marine Invertebrates: A Review.Marine drugs · 2017Review
- Physiological and pathophysiological reactive oxygen species as probed by EPR spectroscopy: the underutilized research window on muscle ageing.The Journal of physiology · 2016Review
- Differential acute and chronic effects of burn trauma on murine skeletal muscle bioenergetics.Burns : journal of the International Society for Burn Injuries · 2016Article
- Serendipity and the discovery of novel compounds that restore mitochondrial plasticity.Clinical pharmacology and therapeutics · 2014Review
- First-in-class cardiolipin-protective compound as a therapeutic agent to restore mitochondrial bioenergetics.British journal of pharmacology · 2014Review
- Redox-optimized ROS balance and the relationship between mitochondrial respiration and ROS.Biochimica et biophysica acta · 2014Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 1 country.
Funding
Abstract
Burn injury causes a major systemic catabolic response that is associated with mitochondrial dysfunction in skeletal muscle. We investigated the effects of the mitochondria-targeted peptide antioxidant Szeto-Schiller 31 (SS-31) on skeletal muscle in a mouse burn model using in vivo phosphorus-31 nuclear magnetic resonance ((31)P NMR) spectroscopy to noninvasively measure high-energy phosphate levels; mitochondrial aconitase activity measurements that directly correlate with TCA cycle flux, as measured by gas chromatography mass spectrometry (GC-MS); and electron paramagnetic resonance (EPR) to assess oxidative stress. At 6 h postburn, the oxidative ATP synthesis rate was increased 5-fold in burned mice given a single dose of SS-31 relative to untreated burned mice (P=0.002). Furthermore, SS-31 administration in burned animals decreased mitochondrial aconitase activity back to control levels. EPR revealed a recovery in redox status of the SS-31-treated burn group compared to the untreated burn group (P<0.05). Our multidisciplinary convergent results suggest that SS-31 promotes recovery of mitochondrial function after burn injury by increasing ATP synthesis rate, improving mitochondrial redox status, and restoring mitochondrial coupling. These findings suggest use of noninvasive in vivo NMR and complementary EPR offers an approach to monitor the effectiveness of mitochondrial protective agents in alleviating burn injury symptoms.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.