ArticleBiophysical journal2009
Modeling cardiac action potential shortening driven by oxidative stress-induced mitochondrial oscillations in guinea pig cardiomyocytes.
Article in Biophysical journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 72 citations in OpenAlex.
- A Computational Model of Oxidative Stress in a Human Ventricular Myocyte.bioRxiv : the preprint server for biology · 2026Article
- A simulation study on the role of mitochondria-sarcoplasmic reticulum CaThe Journal of physiology · 2025Article
- Temporal analysis of doxorubicin-induced cardiac toxicity and hypertrophy.NPJ systems biology and applications · 2025Article
- Metabolic regulation of mitochondrial morphologies in pancreatic beta cells: coupling of bioenergetics and mitochondrial dynamics.Communications biology · 2024Article
- Modeling drug-induced mitochondrial toxicity with human primary cardiomyocytes.Science China. Life sciences · 2024Article
- The age of computational cardiology and future of long-term ablation target prediction for ventricular tachycardia.Frontiers in cardiovascular medicine · 2023Article
- Kinetic Mathematical Modeling of Oxidative Phosphorylation in Cardiomyocyte Mitochondria.Cells · 2022Review
- Modeling Calcium Cycling in the Heart: Progress, Pitfalls, and Challenges.Biomolecules · 2022Review
- Multiscale Modeling of the Mitochondrial Origin of Cardiac Reentrant and Fibrillatory Arrhythmias.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Mitochondria and metabolic transitions in cardiomyocytes: lessons from development for stem cell-derived cardiomyocytes.Stem cell research & therapy · 2021Review
- Variability in electrophysiological properties and conducting obstacles controls re-entry risk in heterogeneous ischaemic tissue.Philosophical transactions. Series A, Mathematical, physical, and engineering sciences · 2020Article
- A Comparative Study of Rat UrineBiology · 2020Article
- Metabolic remodelling of glucose, fatty acid and redox pathways in the heart of type 2 diabetic mice.The Journal of physiology · 2020Article
- Sodium-glucose co-transporter 2 inhibition as a mitochondrial therapy for atrial fibrillation in patients with diabetes?Cardiovascular diabetology · 2020Article
- Diabetes Increases the Vulnerability of the Cardiac Mitochondrial Network to Criticality.Frontiers in physiology · 2020Article
- Quantitative systems models illuminate arrhythmia mechanisms in heart failure: Role of the NaWiley interdisciplinary reviews. Systems biology and medicine · 2019Review
- Mitochondrial chaotic dynamics: Redox-energetic behavior at the edge of stability.Scientific reports · 2018Article
- Mitochondrial-Mediated Oxidative CaJournal of the American Heart Association · 2018Article
- Killing Many Birds With Two Stones: Hypoxia and Fibrosis Can Generate Ectopic Beats in a Human Ventricular Model.Frontiers in physiology · 2018Article
- Mitochondrial Dysfunction-Associated Arrhythmogenic Substrates in Diabetes Mellitus.Frontiers in physiology · 2018Review
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Ischemia-induced shortening of the cardiac action potential and its heterogeneous recovery upon reperfusion are thought to set the stage for reentrant arrhythmias and sudden cardiac death. We have recently reported that the collapse of mitochondrial membrane potential (DeltaPsi(m)) through a mechanism triggered by reactive oxygen species (ROS), coupled to the opening of sarcolemmal ATP-sensitive potassium (K(ATP)) channels, contributes to electrical dysfunction during ischemia-reperfusion. Here we present a computational model of excitation-contraction coupling linked to mitochondrial bioenergetics that incorporates mitochondrial ROS-induced ROS release with coupling between the mitochondrial energy state and electrical excitability mediated by the sarcolemmal K(ATP) current (I(K,ATP)). Whole-cell model simulations demonstrate that increasing the fraction of oxygen diverted from the respiratory chain to ROS production triggers limit-cycle oscillations of DeltaPsi(m), redox potential, and mitochondrial respiration through the activation of a ROS-sensitive inner membrane anion channel. The periods of transient mitochondrial uncoupling decrease the cytosolic ATP/ADP ratio and activate I(K,ATP), consequently shortening the cellular action potential duration and ultimately suppressing electrical excitability. The model simulates emergent behavior observed in cardiomyocytes subjected to metabolic stress and provides a new tool for examining how alterations in mitochondrial oxidative phosphorylation will impact the electrophysiological, contractile, and Ca(2+) handling properties of the cardiac cell. Moreover, the model is an important step toward building multiscale models that will permit investigation of the role of spatiotemporal heterogeneity of mitochondrial metabolism in the mechanisms of arrhythmogenesis and contractile dysfunction in cardiac muscle.
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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.