ArticleAmerican journal of physiology. Heart and circulatory physiology2013
Immediate effects of a single exercise bout on protein O-GlcNAcylation and chromatin regulation of cardiac hypertrophy.
Article in American journal of physiology. Heart and circulatory physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 41 citations in OpenAlex.
- Roles of Glycoproteins in the Diagnosis and Differential Diagnosis of Chronic and Latent Keshan Disease.Molecules (Basel, Switzerland) · 2017Trial
- Seeking the Mechanism for Reversal of Enhanced Insulin Sensitivity After Acute Exercise.Exercise and sport sciences reviews · 2026Review
- The role of protein O-GlcNAcylation in diabetic cardiomyopathy.Biochemical Society transactions · 2024Review
- Roles of O-GlcNAcylation in Mitochondrial Homeostasis and Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2024Review
- Underlying mechanisms of ketotherapy in heart failure: current evidence for clinical implementations.Frontiers in pharmacology · 2024Review
- Metabolite signaling in the heart.Nature cardiovascular research · 2023Review
- The dual role of the hexosamine biosynthetic pathway in cardiac physiology and pathophysiology.Frontiers in endocrinology · 2022Review
- Structure-function relationships and modifications of cardiac sarcoplasmic reticulum Ca2+-transport.Physiological research · 2021Review
- Cardiac Energy Metabolism in Heart Failure.Circulation research · 2021Review
- Role ofPhysiological reviews · 2021Review
- Morphine induces physiological, structural, and molecular benefits in the diabetic myocardium.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
- Energy Metabolism in Exercise-Induced Physiologic Cardiac Hypertrophy.Frontiers in pharmacology · 2020Review
- Glucose Metabolism in Cardiac Hypertrophy and Heart Failure.Journal of the American Heart Association · 2019Review
- Metabolic Coordination of Physiological and Pathological Cardiac Remodeling.Circulation research · 2018Review
- Metabolic Mechanisms of Exercise-Induced Cardiac Remodeling.Frontiers in cardiovascular medicine · 2018Review
- Protein O-GlcNAc Modification Increases in White Blood Cells After a Single Bout of Physical Exercise.Frontiers in immunology · 2018Article
- Involvement of O-GlcNAcylation in the Skeletal Muscle Physiology and Physiopathology: Focus on Muscle Metabolism.Frontiers in endocrinology · 2018Review
- Myocyte membrane and microdomain modifications in diabetes: determinants of ischemic tolerance and cardioprotection.Cardiovascular diabetology · 2017Review
- Exercise training increases protein O-GlcNAcylation in rat skeletal muscle.Physiological reports · 2016Article
- Exercise preferences, levels and quality of life in lung cancer survivors.Supportive care in cancer : official journal of the Multinational Association of Supportive Care in Cancer · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cardiac hypertrophy induced by pathological stimuli is regulated by a complex formed by the repressor element 1-silencing transcription factor (REST) and its corepressor mSin3A. We previously reported that hypertrophic signaling is blunted by O-linked attachment of β-N-acetylglucosamine (O-GlcNAc) to proteins. Regular exercise induces a physiological hypertrophic phenotype in the heart that is associated with decreased O-GlcNAc levels, but a link between O-GlcNAc, the REST complex, and initiation of exercise-induced cardiac hypertrophy is not known. Therefore, mice underwent a single 15- or 30-min bout of moderate- to high-intensity treadmill running, and hearts were harvested immediately and compared with sedentary controls. Cytosolic O-GlcNAc was lower (P < 0.05) following 15 min exercise with no differences in nuclear levels (P > 0.05). There were no differences in cytosolic or nuclear O-GlcNAc levels in hearts after 30 min exercise (P > 0.05). Cellular compartment levels of O-GlcNAc transferase (OGT, the enzyme that removes the O-GlcNAc moiety from proteins), REST, mSin3A, and histone deacetylases (HDACs) 1, 2, 3, 4, and 5 were not changed with exercise. Immunoprecipitation revealed O-GlcNAcylation of OGT and HDACs 1, 2, 4, and 5 that was not changed with acute exercise; however, exercised hearts did exhibit lower interactions between OGT and REST (P < 0.05) but not between OGT and mSin3A. These data suggest that hypertrophic signaling in the heart may be initiated by as little as 15 min of exercise via intracellular changes in protein O-GlcNAcylation distribution and reduced interactions between OGT and the REST chromatin repressor.
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