ArticleCirculation research2011
Exercise protects against myocardial ischemia-reperfusion injury via stimulation of β(3)-adrenergic receptors and increased nitric oxide signaling: role of nitrite and nitrosothiols.
Article in Circulation research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
115 citing papers in PubMed, 200 citations in OpenAlex.
- Trial
- Cardiovascular Protection Variables Based on Exercise Intensity in Stable Coronary Heart Disease Patients After Coronary Stenting: A Comparative Study.Vascular health and risk management · 2020Trial
- Modeling the Exposome in Murine Cardiovascular Disease.JACC. Basic to translational science · 2026Review
- Voluntary wheel running reduces infarct size through thioredoxin-1 and survival pathways.Scientific reports · 2026Article
- Melatonin and mitochondrial protection in cardiac ischemia-reperfusion injury: mechanisms, evidence and translational perspectives.Basic research in cardiology · 2026Review
- Understanding Exercise-induced Protection in Heart Failure with Reduced Ejection Fraction and Heart Failure with Preserved Ejection Fraction: Molecular Mechanisms and New Therapeutic Opportunities.Cardiac failure review · 2026Review
- Therapeutic Potential of the β3-Adrenergic Receptor and Its Ligands in Cardiovascular Diseases.International journal of molecular sciences · 2025Review
- Expert consensus statement for basic research of animal exercise intervention studies in chronic disease prevention and treatment: A joint position paper of the Exercise Science branch of the Biophysical Society of China and the Metabolism and Genetics branch of the Genetics Society of China.Journal of sport and health science · 2025Article
- High-intensity interval training improves mitochondrial function and attenuates cardiomyocytes damage in ischemia-reperfusion.International journal of cardiology. Heart & vasculature · 2025Review
- Moderate-intensity interval exercise exacerbates cardiac lipotoxicity in high-fat, high-calories diet-fed mice.Nature communications · 2025Article
- An overview of the multi-dimensional mechanisms of exercise-regulated hormones and growth factors in cardiac physiological adaptation.Frontiers in physiology · 2025Review
- Regulating the expression of exercise-induced micro-RNAs and long non-coding RNAs: implications for controlling cardiovascular diseases and heart failure.Frontiers in molecular biosciences · 2025Review
- β3-Adrenergic receptor overexpression in cardiomyocytes preconditions mitochondria to withstand ischemia-reperfusion injury.Basic research in cardiology · 2024Article
- Post-Ischemic Stroke Cardiovascular Risk Prevention and Management.Healthcare (Basel, Switzerland) · 2024Review
- Exercise-induced cardiac mitochondrial reorganization and enhancement in spontaneously hypertensive rats.Pflugers Archiv : European journal of physiology · 2024Article
- Intrinsic and Extrinsic Contributors to the Cardiac Benefits of Exercise.JACC. Basic to translational science · 2024Review
- Inside the Biology of the β3-Adrenoceptor.Biomolecules · 2024Review
- Exercise Training Decreases Nitrite Concentration in the Heart and Locomotory Muscles of Rats Without Changing the Muscle Nitrate Content.Journal of the American Heart Association · 2024Article
- Cardiac optogenetics: shining light on signaling pathways.Pflugers Archiv : European journal of physiology · 2023Review
- Is Intrinsic Cardioprotection a Laboratory Phenomenon or a Clinically Relevant Tool to Salvage the Failing Heart?International journal of molecular sciences · 2023Review
55 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
rationaleExercise training confers sustainable protection against ischemia-reperfusion injury in animal models and has been associated with improved survival following a heart attack in humans. It is still unclear how exercise protects the heart, but it is apparent that endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) play a role.
objectiveTo determine the role of β(3)-adrenergic receptors (β(3)-ARs), eNOS activation, and NO metabolites (nitrite and nitrosothiols) in the sustained cardioprotective effects of exercise. METHODS AND
resultsHere we show that voluntary exercise reduces myocardial injury in mice following a 4-week training period and that these protective effects can be sustained for at least 1 week following the cessation of the training. The sustained cardioprotective effects of exercise are mediated by alterations in the phosphorylation status of eNOS (increase in serine 1177 and decrease in threonine 495), leading to an increase in NO generation and storage of NO metabolites (nitrite and nitrosothiols) in the heart. Further evidence revealed that the alterations in eNOS phosphorylation status and NO generation were mediated by β(3)-AR stimulation and that in response to exercise a deficiency of β(3)-ARs leads to an exacerbation of myocardial infarction following ischemia-reperfusion injury.
conclusionsOur findings clearly demonstrate that exercise protects the heart against myocardial ischemia-reperfusion injury by stimulation of β(3)-ARs and increased cardiac storage of nitric oxide metabolites (ie, nitrite and nitrosothiols).
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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.