ArticleThe Journal of physiology2013
Novel role for thioredoxin reductase-2 in mitochondrial redox adaptations to obesogenic diet and exercise in heart and skeletal muscle.
Article in The Journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 63 citations in OpenAlex.
- Do fish oil omega-3 fatty acids enhance antioxidant capacity and mitochondrial fatty acid oxidation in human atrial myocardium via PPARγ activation?Antioxidants & redox signaling · 2014Trial
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- Physical-Exercise-Induced Antioxidant Effects on the Brain and Skeletal Muscle.Antioxidants (Basel, Switzerland) · 2022Review
- Skeletal myopathy in a rat model of postmenopausal heart failure with preserved ejection fraction.Journal of applied physiology (Bethesda, Md. : 1985) · 2022Article
- Pathways Linking Nicotinamide Adenine Dinucleotide Phosphate Production to Endoplasmic Reticulum Protein Oxidation and Stress.Frontiers in molecular biosciences · 2022Review
- Cardiac robustness regulated by reactive sulfur species.Journal of clinical biochemistry and nutrition · 2022Article
- Prohibitin-1 Is a Dynamically Regulated Blood Protein With Cardioprotective Effects in Sepsis.Journal of the American Heart Association · 2021Article
- Exercise triggers CAPN1-mediated AIF truncation, inducing myocyte cell death in arrhythmogenic cardiomyopathy.Science translational medicine · 2021Article
- Diabetes Mellitus, Mitochondrial Dysfunction and CaInternational journal of molecular sciences · 2020Review
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- Chronic kidney disease exacerbates ischemic limb myopathy in mice via altered mitochondrial energetics.Scientific reports · 2019Article
- Early myopathy in Duchenne muscular dystrophy is associated with elevated mitochondrial HJournal of cachexia, sarcopenia and muscle · 2019Article
- Mitochondrial accumulation of doxorubicin in cardiac and diaphragm muscle following exercise preconditioning.Mitochondrion · 2019Article
- 3-Weeks of Exercise Training Increases Ischemic-Tolerance in Hearts From High-Fat Diet Fed Mice.Frontiers in physiology · 2019Article
- Induction of fat apoptosis by a non-thermal device: Mechanism of action of non-invasive high-intensity electromagnetic technology in a porcine model.Lasers in surgery and medicine · 2019Article
- A carnosine analog mitigates metabolic disorders of obesity by reducing carbonyl stress.The Journal of clinical investigation · 2018Article
- Mitochondrial Diagnostics: A Multiplexed Assay Platform for Comprehensive Assessment of Mitochondrial Energy Fluxes.Cell reports · 2018Article
- The role of the thioredoxin/thioredoxin reductase system in the metabolic syndrome: towards a possible prognostic marker?Cellular and molecular life sciences : CMLS · 2018Review
- Alterations in fatty acid metabolism and sirtuin signaling characterize early type-2 diabetic hearts of fructose-fed rats.Physiological reports · 2017Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Increased fatty acid availability and oxidative stress are physiological consequences of exercise (Ex) and a high-fat, high-sugar (HFHS) diet. Despite these similarities, the global effects of Ex are beneficial, whereas HFHS diets are largely deleterious to the cardiovascular system. The reasons for this disparity are multifactorial and incompletely understood. We hypothesized that differences in redox adaptations following HFHS diet in comparison to exercise may underlie this disparity, particularly in mitochondria. Our objective in this study was to determine mechanisms by which heart and skeletal muscle (red gastrocnemius, RG) mitochondria experience differential redox adaptations to 12 weeks of HFHS diet and/or exercise training (Ex) in rats. Surprisingly, both HFHS feeding and Ex led to contrasting effects in heart and RG, in that mitochondrial H2O2 decreased in heart but increased in RG following both HFHS diet and Ex, in comparison to sedentary animals fed a control diet. These differences were determined to be due largely to increased antioxidant/anti-inflammatory enzymes in the heart following the HFHS diet, which did not occur in RG. Specifically, upregulation of mitochondrial thioredoxin reductase-2 occurred with both HFHS and Ex in the heart, but only with Ex in RG, and systematic evaluation of this enzyme revealed that it is critical for suppressing mitochondrial H2O2 during fatty acid oxidation. These findings are novel and important in that they illustrate the unique ability of the heart to adapt to oxidative stress imposed by HFHS diet, in part through upregulation of thioredoxin reductase-2. Furthermore, upregulation of thioredoxin reductase-2 plays a critical role in preserving the mitochondrial redox status in the heart and skeletal muscle with exercise.
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Registered trials
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