ReviewOxidative medicine and cellular longevity2016
The Role of Mitochondrial Reactive Oxygen Species in Cardiovascular Injury and Protective Strategies.
Review in Oxidative medicine and cellular longevity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.
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Who cites it
67 citing papers in PubMed, 118 citations in OpenAlex.
- Medicinal Plants and Phytochemicals in Cardioprotection-Mechanistic Pathways and Translational Roadmap.Life (Basel, Switzerland) · 2026Review
- Corticotropin-releasing factor (CRF) in brain aging: from mitochondrial dysfunction to inflammaging.Frontiers in aging neuroscience · 2026Review
- Monoamine oxidases are mediators of oxidative stress in human varicose Veins: interactions with obesity, inflammation, and angiotensin II.Molecular and cellular biochemistry · 2026Article
- High-intensity interval training improves mitochondrial function and attenuates cardiomyocytes damage in ischemia-reperfusion.International journal of cardiology. Heart & vasculature · 2025Review
- How to measure and model cardiovascular aging.Cardiovascular research · 2025Review
- Oxidative Stress in the Pathophysiology of Chronic Venous Disease: An Overview.Antioxidants (Basel, Switzerland) · 2025Review
- Mitochondrial Dysfunction and Oxidative Stress: Emerging Insights in Muscle and Cardiovascular Disease Mechanisms.Antioxidants (Basel, Switzerland) · 2025Article
- Mitochondrial dysfunction in the regulation of aging and aging-related diseases.Cell communication and signaling : CCS · 2025Review
- Mitochondrial Dysfunction in Cardiac Surgery.Anesthesiology clinics · 2025Review
- Combining RNA-seq, molecular docking and experimental verification to explore the mechanism of BAM15 as a potential drug for atherosclerosis.Scientific reports · 2025Article
- Empagliflozin and dapagliflozin decreased atrial monoamine oxidase expression and alleviated oxidative stress in overweight non-diabetic cardiac patients.Molecular and cellular biochemistry · 2025Article
- Mitochondrial complex-1 as a therapeutic target for cardiac diseases.Molecular and cellular biochemistry · 2025Review
- Liver and Pancreatic Toxicity of Endocrine-Disruptive Chemicals: Focus on Mitochondrial Dysfunction and Oxidative Stress.International journal of molecular sciences · 2024Review
- Dose-dependent effects of acetaminophen and ibuprofen on mitochondrial respiration of human platelets.Molecular and cellular biochemistry · 2024Article
- Oleuropein alleviates myocardial ischemia-reperfusion injury by suppressing oxidative stress and excessive autophagy via TLR4/MAPK signaling pathway.Chinese medicine · 2024Article
- Regenerative loss in the animal kingdom as viewed from the mouse digit tip and heart.Developmental biology · 2024Review
- Advances in pathogenesis and treatment of vascular endothelial injury-related diseases mediated by mitochondrial abnormality.Frontiers in pharmacology · 2024Review
- Protective Effect of Uridine on Structural and Functional Rearrangements in Heart Mitochondria after a High-Dose Isoprenaline Exposure Modelling Stress-Induced Cardiomyopathy in Rats.International journal of molecular sciences · 2023Article
- Comparative Analysis of Heart Regeneration: Searching for the Key to Heal the Heart-Part II: Molecular Mechanisms of Cardiac Regeneration.Journal of cardiovascular development and disease · 2023Review
- Monoamine Oxidase (MAO) Is Expressed at the Level of Mitral Valve with Severe Regurgitation in Hypertrophic Obstructive Cardiomyopathy: A Case Report.Medicina (Kaunas, Lithuania) · 2022Article
7 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ischaemia/reperfusion (I/R) injury of the heart represents a major health burden mainly associated with acute coronary syndromes. While timely coronary reperfusion has become the established routine therapy in patients with ST-elevation myocardial infarction, the restoration of blood flow into the previously ischaemic area is always accompanied by myocardial injury. The central mechanism involved in this phenomenon is represented by the excessive generation of reactive oxygen species (ROS). Besides their harmful role when highly generated during early reperfusion, minimal ROS formation during ischaemia and/or at reperfusion is critical for the redox signaling of cardioprotection. In the past decades, mitochondria have emerged as the major source of ROS as well as a critical target for cardioprotective strategies at reperfusion. Mitochondria dysfunction associated with I/R myocardial injury is further described and ultimately analyzed with respect to its role as source of both deleterious and beneficial ROS. Furthermore, the contribution of ROS in the highly investigated field of conditioning strategies is analyzed. In the end, the vascular sources of mitochondria-derived ROS are briefly reviewed.
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