ArticleBasic research in cardiology2021
Increased protein S-nitrosylation in mitochondria: a key mechanism of exercise-induced cardioprotection.
Article in Basic research in cardiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Protein S-nitrosylation in the heart: Mechanisms, physiological roles, and pathological remodeling.Redox biology · 2026Review
- Review
- Exploring the role of CaMKII in exercise-induced cardioprotection.Human cell · 2026Review
- Melatonin and mitochondrial protection in cardiac ischemia-reperfusion injury: mechanisms, evidence and translational perspectives.Basic research in cardiology · 2026Review
- Exercise modulates redox homeostasis in cardiovascular and metabolic diseases: from bench to clinic.Cardiovascular diabetology · 2026Review
- High-Intensity Interval Training Attenuates Inflammation in Cardiorenal Syndrome Induced by Renal Ischemia-Reperfusion Injury in Rats.Life (Basel, Switzerland) · 2025Article
- Exercise training for myocardial ischemia reperfusion injury: Mechanism and clinical practice (Review).International journal of molecular medicine · 2025Review
- The regulatory role of exercise in heart failure and myocardial energy metabolism: A review.Biomolecules & biomedicine · 2025Review
- Metabolic Alterations Associated With Right Ventricular Dysfunction in Pulmonary Arterial Hypertension: The Modulatory Effects and Improvement Mechanisms of Exercise.Reviews in cardiovascular medicine · 2025Review
- Mitochondrial Dysfunction in HFpEF: Potential Interventions Through Exercise.Journal of cardiovascular translational research · 2025Review
- Subcellular Localization Guides eNOS Function.International journal of molecular sciences · 2024Review
- Exercise training may reduce fragmented mitochondria in the ischemic-reperfused heart through DRP1.The Journal of general physiology · 2024Article
- Mechanisms and benefits of cardiac rehabilitation in individuals with stroke: emerging role of its impact on improving cardiovascular and neurovascular health.Frontiers in cardiovascular medicine · 2024Review
- Cardioprotective Strategies After Ischemia-Reperfusion Injury.American journal of cardiovascular drugs : drugs, devices, and other interventions · 2024Review
- Mitochondrial Dysfunction in Cardiotoxicity Induced by BCR-ABL1 Tyrosine Kinase Inhibitors -Underlying Mechanisms, Detection, Potential Therapies.Cardiovascular toxicology · 2023Review
- Protective Role of Chronic Exercise Training in Modulating the Impact of Hyperglycemia on Vascular Sensitivity to Ischemia-Reperfusion.Nutrients · 2023Article
- Exercise training maintains cardiovascular health: signaling pathways involved and potential therapeutics.Signal transduction and targeted therapy · 2022Review
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Authors and funding
11 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelial nitric oxide synthase (eNOS) activation in the heart plays a key role in exercise-induced cardioprotection during ischemia-reperfusion, but the underlying mechanisms remain unknown. We hypothesized that the cardioprotective effect of exercise training could be explained by the re-localization of eNOS-dependent nitric oxide (NO)/S-nitrosylation signaling to mitochondria. By comparing exercised (5 days/week for 5 weeks) and sedentary Wistar rats, we found that exercise training increased eNOS level and activation by phosphorylation (at serine 1177) in mitochondria, but not in the cytosolic subfraction of cardiomyocytes. Using confocal microscopy, we confirmed that NO production in mitochondria was increased in response to H
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