ArticleBiophysical journal2013
A computational model of reactive oxygen species and redox balance in cardiac mitochondria.
Article in Biophysical journal, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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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
33 citing papers in PubMed, 58 citations in OpenAlex.
- A Computational Model of Oxidative Stress in a Human Ventricular Myocyte.bioRxiv : the preprint server for biology · 2026Article
- Unlocking mitochondrial dysfunction-associated senescence (MiDAS) with NADTranslational oncology · 2024Article
- Oxidative Stress in Sepsis: A Focus on Cardiac Pathology.International journal of molecular sciences · 2024Article
- Calcium and Reactive Oxygen Species Signaling Interplays in Cardiac Physiology and Pathologies.Antioxidants (Basel, Switzerland) · 2023Review
- Computational Modeling of Substrate-Dependent Mitochondrial Respiration and Bioenergetics in the Heart and Kidney Cortex and Outer Medulla.Function (Oxford, England) · 2023Article
- Kinetic Mathematical Modeling of Oxidative Phosphorylation in Cardiomyocyte Mitochondria.Cells · 2022Review
- A computational model of cardiomyocyte metabolism predicts unique reperfusion protocols capable of reducing cell damage during ischemia/reperfusion.The Journal of biological chemistry · 2022Article
- Computational Models on Pathological Redox Signalling Driven by Pregnancy: A Review.Antioxidants (Basel, Switzerland) · 2022Review
- Mitochondrial CaInternational journal of molecular sciences · 2022Review
- Identifying Site-Specific Superoxide and Hydrogen Peroxide Production Rates From the Mitochondrial Electron Transport System Using a Computational Strategy.Function (Oxford, England) · 2021Article
- In Sickness and in Health: The Oxygen Reactive Species and the Bone.Frontiers in bioengineering and biotechnology · 2021Review
- Network integration and modelling of dynamic drug responses at multi-omics levels.Communications biology · 2020Article
- Hydrogen peroxide diffusion and scavenging shapes mitochondrial network instability and failure by sensitizing ROS-induced ROS release.Scientific reports · 2020Article
- Mitochondrial CaMKII causes adverse metabolic reprogramming and dilated cardiomyopathy.Nature communications · 2020Article
- Modelling mitochondrial ROS production by the respiratory chain.Cellular and molecular life sciences : CMLS · 2020Review
- Quantitative systems models illuminate arrhythmia mechanisms in heart failure: Role of the NaWiley interdisciplinary reviews. Systems biology and medicine · 2019Review
- Cardiac-specific Conditional Knockout of the 18-kDa Mitochondrial Translocator Protein Protects from Pressure Overload Induced Heart Failure.Scientific reports · 2018Article
- Analysis of a Functional Dimer Model of Ubiquinol Cytochrome c Oxidoreductase.Biophysical journal · 2017Article
- Modeling oxygen requirements in ischemic cardiomyocytes.The Journal of biological chemistry · 2017Article
- Endogenous nitric oxide formation in cardiac myocytes does not control respiration during β-adrenergic stimulation.The Journal of physiology · 2017Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Elevated levels of reactive oxygen species (ROS) play a critical role in cardiac myocyte signaling in both healthy and diseased cells. Mitochondria represent the predominant cellular source of ROS, specifically the activity of complexes I and III. The model presented here explores the modulation of electron transport chain ROS production for state 3 and state 4 respiration and the role of substrates and respiratory inhibitors. Model simulations show that ROS production from complex III increases exponentially with membrane potential (ΔΨm) when in state 4. Complex I ROS release in the model can occur in the presence of NADH and succinate (reverse electron flow), leading to a highly reduced ubiquinone pool, displaying the highest ROS production flux in state 4. In the presence of ample ROS scavenging, total ROS production is moderate in state 3 and increases substantially under state 4 conditions. The ROS production model was extended by combining it with a minimal model of ROS scavenging. When the mitochondrial redox status was oxidized by increasing the proton permeability of the inner mitochondrial membrane, simulations with the combined model show that ROS levels initially decline as production drops off with decreasing ΔΨm and then increase as scavenging capacity is exhausted. Hence, this mechanistic model of ROS production demonstrates how ROS levels are controlled by mitochondrial redox balance.
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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.