ArticleBiophysical journal2013
Integrating mitochondrial energetics, redox and ROS metabolic networks: a two-compartment model.
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 61 papers.
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Who cites it
61 citing papers in PubMed, 102 citations in OpenAlex.
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- Tafazzin deficiency causes substantial remodeling in the lipidome of a mouse model of Barth Syndrome cardiomyopathy.Frontiers in molecular medicine · 2024Article
- Prospects of potential adipokines as therapeutic agents in obesity-linked atherogenic dyslipidemia and insulin resistance.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 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
- Quantitative modeling of pentose phosphate pathway response to oxidative stress reveals a cooperative regulatory strategy.iScience · 2022Article
- Digitoxin Affects Metabolism, ROS Production and Proliferation in Pancreatic Cancer Cells Differently Depending on the Cell Phenotype.International journal of molecular sciences · 2022Article
- The Modulatory Role of sti-1 in Methylmercury-Induced Toxicity in Caenorhabditis elegans.Neurotoxicity research · 2022Article
- Computational modeling of mitochondrial KJournal of molecular and cellular cardiology · 2022Article
- Mitochondrial CaInternational journal of molecular sciences · 2022Review
- Computational Approaches and Tools as Applied to the Study of Rhythms and Chaos in Biology.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Mitochondrial remodelling-a vicious cycle in diabetic complications.Molecular biology reports · 2021Review
- Oxidative Stress Evaluation in Ischemia Reperfusion Models: Characteristics, Limits and Perspectives.International journal of molecular sciences · 2021Review
- Mitochondrial CaJournal of molecular and cellular cardiology · 2021Review
- Identifying Site-Specific Superoxide and Hydrogen Peroxide Production Rates From the Mitochondrial Electron Transport System Using a Computational Strategy.Function (Oxford, England) · 2021Article
- Computationally modeling mammalian succinate dehydrogenase kinetics identifies the origins and primary determinants of ROS production.The Journal of biological chemistry · 2020Article
- Hydrogen peroxide diffusion and scavenging shapes mitochondrial network instability and failure by sensitizing ROS-induced ROS release.Scientific reports · 2020Article
1 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
To understand the mechanisms involved in the control and regulation of mitochondrial reactive oxygen species (ROS) levels, a two-compartment computational mitochondrial energetic-redox (ME-R) model accounting for energetic, redox, and ROS metabolisms is presented. The ME-R model incorporates four main redox couples (NADH/NAD(+), NADPH/NADP(+), GSH/GSSG, Trx(SH)(2)/TrxSS). Scavenging systems-glutathione, thioredoxin, superoxide dismutase, catalase-are distributed in mitochondrial matrix and extra-matrix compartments, and transport between compartments of ROS species (superoxide: O(2)(⋅-), hydrogen peroxide: H(2)O(2)), and GSH is also taken into account. Model simulations are compared with experimental data obtained from isolated heart mitochondria. The ME-R model is able to simulate: i), the shape and order of magnitude of H(2)O(2) emission and dose-response kinetics observed after treatment with inhibitors of the GSH or Trx scavenging systems and ii), steady and transient behavior of ΔΨ(m) and NADH after single or repetitive pulses of substrate- or uncoupler-elicited energetic-redox transitions. The dynamics of the redox environment in both compartments is analyzed with the model following substrate addition. The ME-R model represents a useful computational tool for exploring ROS dynamics, the role of compartmentation in the modulation of the redox environment, and how redox regulation participates in the control of mitochondrial function.
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