ArticleAmerican journal of physiology. Heart and circulatory physiology2013
Mitochondrial reactive oxygen species: which ROS signals cardioprotection?
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 36 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.
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Who cites it
36 citing papers in PubMed, 60 citations in OpenAlex.
- Repurposed cAMP-Modulating Agents Enhance 5-Fluorouracil Response Through Membrane-Dependent Mechanisms.Membranes · 2026Review
- Medicinal Plants and Phytochemicals in Cardioprotection-Mechanistic Pathways and Translational Roadmap.Life (Basel, Switzerland) · 2026Review
- Ion channels and cardiac disease: mechanisms and functions of a disintegrin and metalloproteases and their substrates.Frontiers in cell and developmental biology · 2026Review
- The multifaceted role of mitochondria in cardiac function: insights and approaches.Cell communication and signaling : CCS · 2024Review
- Mitochondrial Cristae Morphology Reflecting Metabolism, Superoxide Formation, Redox Homeostasis, and Pathology.Antioxidants & redox signaling · 2023Review
- Mitochondrial Volume Regulation and Swelling Mechanisms in Cardiomyocytes.Antioxidants (Basel, Switzerland) · 2023Review
- Endothelial Function and Hypoxic-Hyperoxic Preconditioning in Coronary Surgery with a Cardiopulmonary Bypass: Randomized Clinical Trial.Biomedicines · 2023Article
- Specific Features of Mitochondrial Dysfunction under Conditions of Ferroptosis Induced byMembranes · 2023Article
- The Ambivalence of Connexin43 Gap Peptides in Cardioprotection of the Isolated Heart against Ischemic Injury.International journal of molecular sciences · 2022Article
- Article
- Antioxidant Synergy of Mitochondrial Phospholipase PNPLA8/iPLA2γ with Fatty Acid-Conducting SLC25 Gene Family Transporters.Antioxidants (Basel, Switzerland) · 2021Review
- Identifying Site-Specific Superoxide and Hydrogen Peroxide Production Rates From the Mitochondrial Electron Transport System Using a Computational Strategy.Function (Oxford, England) · 2021Article
- Diazoxide and Exercise Enhance Muscle Contraction during Obesity by Decreasing ROS Levels, Lipid Peroxidation, and Improving Glutathione Redox Status.Antioxidants (Basel, Switzerland) · 2020Article
- Nicorandil Affects Mitochondrial Respiratory Chain Function by Increasing Complex III Activity and ROS Production in Skeletal Muscle Mitochondria.The Journal of membrane biology · 2020Article
- Influence of Hypoxic and Hyperoxic Preconditioning on Endothelial Function in a Model of Myocardial Ischemia-Reperfusion Injury with Cardiopulmonary Bypass (Experimental Study).International journal of molecular sciences · 2020Article
- Intermittent Hypoxia Augments Pulmonary Vasoconstrictor Reactivity through PKCβ/Mitochondrial Oxidant Signaling.American journal of respiratory cell and molecular biology · 2020Article
- Review
- Redox Signaling from Mitochondria: Signal Propagation and Its Targets.Biomolecules · 2020Review
- SARS-CoV-2 Mediated Endothelial Dysfunction: The Potential Role of Chronic Oxidative Stress.Frontiers in physiology · 2020Review
- Recent Advances in Pharmacological and Non-Pharmacological Strategies of Cardioprotection.International journal of molecular sciences · 2019Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Mitochondria are the major effectors of cardioprotection by procedures that open the mitochondrial ATP-sensitive potassium channel (mitoKATP), including ischemic and pharmacological preconditioning. MitoKATP opening leads to increased reactive oxygen species (ROS), which then activate a mitoKATP-associated PKCε, which phosphorylates mitoKATP and leaves it in a persistent open state (Costa AD, Garlid KD. Am J Physiol Heart Circ Physiol 295, H874-H882, 2008). The ROS responsible for this effect is not known. The present study focuses on superoxide (O2(·-)), hydrogen peroxide (H2O2), and hydroxyl radical (HO(·)), each of which has been proposed as the signaling ROS. Feedback activation of mitoKATP provides an ideal setting for studying endogenous ROS signaling. Respiring rat heart mitochondria were preincubated with ATP and diazoxide, together with an agent being tested for interference with this process, either by scavenging ROS or by blocking ROS transformations. The mitochondria were then assayed to determine whether or not the persistent phosphorylated open state was achieved. Dimethylsulfoxide (DMSO), dimethylformamide (DMF), deferoxamine, Trolox, and bromoenol lactone each interfered with formation of the ROS-dependent open state. Catalase did not interfere with this step. We also found that DMF blocked cardioprotection by both ischemic preconditioning and diazoxide. The lack of a catalase effect and the inhibitory effects of agents acting downstream of HO(·) excludes H2O2 as the endogenous signaling ROS. Taken together, the results support the conclusion that the ROS message is carried by a downstream product of HO(·) and that it is probably a product of phospholipid oxidation.
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Registered trials
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