ArticleTranslational research : the journal of laboratory and clinical medicine2012
Blockade of electron transport before ischemia protects mitochondria and decreases myocardial injury during reperfusion in aged rat hearts.
Article in Translational research : the journal of laboratory and clinical medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- Mitochondrial function in intestinal ischemia-reperfusion injury: mechanisms and therapeutic perspectives.Molecular biology reports · 2025Review
- Metabolic landscape in cardiac aging: insights into molecular biology and therapeutic implications.Signal transduction and targeted therapy · 2023Review
- Recombinant Adenovirus siRNA Knocking Down the Ndufs4 Gene Alleviates Myocardial Apoptosis Induced by Oxidative Stress Injury.Cardiology research and practice · 2023Article
- Reversing mitochondrial defects in aged hearts: role of mitochondrial calpain activation.American journal of physiology. Cell physiology · 2022Article
- Calpain-mediated protein targets in cardiac mitochondria following ischemia-reperfusion.Scientific reports · 2022Article
- Therapeutic Targets for Regulating Oxidative Damage Induced by Ischemia-Reperfusion Injury: A Study from a Pharmacological Perspective.Oxidative medicine and cellular longevity · 2022Review
- Article
- Preventing Myocardial Injury Following Non-Cardiac Surgery: A Potential Role for Preoperative Antioxidant Therapy with Ubiquinone.Antioxidants (Basel, Switzerland) · 2021Review
- Mitochondrial Metabolism in Myocardial Remodeling and Mechanical Unloading: Implications for Ischemic Heart Disease.Frontiers in cardiovascular medicine · 2021Review
- Targeting ER stress and calpain activation to reverse age-dependent mitochondrial damage in the heart.Mechanisms of ageing and development · 2020Review
- Neutrophil-Mediated Cardiac Damage After Acute Myocardial Infarction: Significance of Defining a New Target Cell Type for Developing Cardioprotective Drugs.Antioxidants & redox signaling · 2020Article
- Ischemia and reperfusion injury to mitochondria and cardiac function in donation after circulatory death hearts- an experimental study.PloS one · 2020Article
- Ischemia/Reperfusion Injury Revisited: An Overview of the Latest Pharmacological Strategies.International journal of molecular sciences · 2019Review
- Intermediary metabolism and fatty acid oxidation: novel targets of electron transport chain-driven injury during ischemia and reperfusion.American journal of physiology. Heart and circulatory physiology · 2018Article
- The Effects of Potassium Cyanide on the Functional Recovery of Isolated Rat Hearts after Ischemia and Reperfusion: The Role of Oxidative Stress.Oxidative medicine and cellular longevity · 2018Article
- Inhibiting Cytochrome C Oxidase Leads to Alleviated Ischemia Reperfusion Injury.Korean circulation journal · 2017Article
- Mitochondrial Dysfunction and Myocardial Ischemia-Reperfusion: Implications for Novel Therapies.Annual review of pharmacology and toxicology · 2017Review
- Bone marrow-derived mesenchymal stem cells rescue injured H9c2 cells via transferring intact mitochondria through tunneling nanotubes in an in vitro simulated ischemia/reperfusion model.Molecular medicine reports · 2016Article
- The Role of Oxidative Stress in Myocardial Ischemia and Reperfusion Injury and Remodeling: Revisited.Oxidative medicine and cellular longevity · 2016Review
- Translational Regulation of the Mitochondrial Genome Following Redistribution of Mitochondrial MicroRNA in the Diabetic Heart.Circulation. Cardiovascular genetics · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Myocardial injury is increased in the aged heart following ischemia and reperfusion (I-R) in both humans and experimental models. Hearts from aged 24-month-old Fischer 344 rats sustain greater cell death and decreased contractile recovery after I-R compared with 6-month-old adult controls. Cardiac mitochondria incur damage during I-R contributing to cell death. Aged rats have a defect in complex III of the mitochondrial electron transport chain (ETC) localized to the interfibrillar population of cardiac mitochondria (IFM), situated in the interior of the cardiomyocyte among the myofibrils. The defect involves the quinol oxidation site (Qo) and increases the production of reactive oxygen species (ROS) in the baseline state. Ischemia further decreases complex III activity via functional inactivation of the iron-sulfur subunit. We studied the contribution of ischemia-induced defects in complex III with the increased cardiac injury in the aged heart. The reversible blockade of the ETC proximal to complex III during ischemia using amobarbital protects mitochondria against ischemic damage, removing the ischemia component of mitochondrial dysfunction. Reperfusion of the aged heart in the absence of ischemic mitochondrial damage decreases net ROS production from mitochondria and reduces cell death. Thus, even despite the persistence of the age-related defects in electron transport, protection against ischemic damage to mitochondria can reduce injury in the aged heart. The direct therapeutic targeting of mitochondria protects against ischemic damage and decreases cardiac injury during reperfusion in the high risk elderly heart.
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Registered trials
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