ArticleBiophysical journal2016
Catalytic Coupling of Oxidative Phosphorylation, ATP Demand, and Reactive Oxygen Species Generation.
Article in Biophysical journal, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed.
- Preliminary study of polyethylene microplastics disrupting energy Metabolism, redox Balance, and prefrontal cortex structure in Wistar rats.Scientific reports · 2026Article
- Integrating simulated and experimental data to identify mitochondrial bioenergetic defects in Parkinson's Disease models.PloS one · 2026Article
- A simulation study on the role of mitochondria-sarcoplasmic reticulum CaThe Journal of physiology · 2025Article
- Unlocking mitochondrial dysfunction-associated senescence (MiDAS) with NADTranslational oncology · 2024Article
- Guidelines for mechanistic modeling and analysis in cardiovascular research.American journal of physiology. Heart and circulatory physiology · 2024Review
- Postnatal growth restriction alters myocardial mitochondrial energetics in mice.Experimental physiology · 2024Article
- Integrated Functions of Cardiac Energetics, Mechanics, and Purine Nucleotide Metabolism.Comprehensive Physiology · 2023Article
- Crosstalk between adenine nucleotide transporter and mitochondrial swelling: experimental and computational approaches.Cell biology and toxicology · 2023Article
- 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
- Single-cell RNA-seq uncovered hemocyte functional subtypes and their differentiational characteristics and connectivity with morphological subpopulations inFrontiers in immunology · 2022Article
- Quantitative analysis of mitochondrial ATP synthesis.Mathematical biosciences · 2021Article
- Network Thermodynamical Modeling of Bioelectrical Systems: A Bond Graph Approach.Bioelectricity · 2021Article
- 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
- Modelling mitochondrial ROS production by the respiratory chain.Cellular and molecular life sciences : CMLS · 2020Review
- Brain Metabolism Monitoring through CCO Measurements Using All-Fiber-Integrated Super-Continuum Source.Proceedings of SPIE--the International Society for Optical Engineering · 2020Article
- A model of mitochondrial OAmerican journal of physiology. Renal physiology · 2020Article
- Impaired Myocardial Energetics Causes Mechanical Dysfunction in Decompensated Failing Hearts.Function (Oxford, England) · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Competing models of mitochondrial energy metabolism in the heart are highly disputed. In addition, the mechanisms of reactive oxygen species (ROS) production and scavenging are not well understood. To deepen our understanding of these processes, a computer model was developed to integrate the biophysical processes of oxidative phosphorylation and ROS generation. The model was calibrated with experimental data obtained from isolated rat heart mitochondria subjected to physiological conditions and workloads. Model simulations show that changes in the quinone pool redox state are responsible for the apparent inorganic phosphate activation of complex III. Model simulations predict that complex III is responsible for more ROS production during physiological working conditions relative to complex I. However, this relationship is reversed under pathological conditions. Finally, model analysis reveals how a highly reduced quinone pool caused by elevated levels of succinate is likely responsible for the burst of ROS seen during reperfusion after ischemia.
Indexed as
Identifiers
What OpenQuestion holds
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.