ArticleAmerican journal of physiology. Heart and circulatory physiology2012
Mathematical modeling mechanisms of arrhythmias in transgenic mouse heart overexpressing TNF-α.
Article in American journal of physiology. Heart and circulatory physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 29 citations in OpenAlex.
- Optogenetic quantification of cardiac excitability and electrical coupling in intact hearts to explain cardiac arrhythmia initiation.Science advances · 2025Article
- In silico optical modulation of spiral wave trajectories in cardiac tissue.Pflugers Archiv : European journal of physiology · 2023Article
- Dissolution of spiral wave's core using cardiac optogenetics.PLoS computational biology · 2023Article
- Mechanism of Datura metel on sinus bradycardia based on network pharmacology and molecular docking.Medicine · 2022Article
- Optogenetic manipulation of cardiac electrical dynamics using sub-threshold illumination: dissecting the role of cardiac alternans in terminating rapid rhythms.Basic research in cardiology · 2022Article
- A move in the light direction.eLife · 2021Article
- Article
- Review
- Lack of Macrophage Migration Inhibitory Factor Reduces Susceptibility to Ventricular Arrhythmias During the Acute Phase of Myocardial Infarction.Journal of inflammation research · 2021Article
- Complexity of TNF-α Signaling in Heart Disease.Journal of clinical medicine · 2020Review
- A compartmentalized mathematical model of mouse atrial myocytes.American journal of physiology. Heart and circulatory physiology · 2020Article
- A Mathematical Model of the Human Cardiac NaThe Journal of membrane biology · 2019Article
- Bursting dynamics in the normal and failing hearts.Scientific reports · 2017Article
- Effect of lysophosphatidic acid on the immune inflammatory response and the connexin 43 protein in myocardial infarction.Experimental and therapeutic medicine · 2016Article
- Ryanodine receptor sensitivity governs the stability and synchrony of local calcium release during cardiac excitation-contraction coupling.Journal of molecular and cellular cardiology · 2016Article
- Involvement of Inflammatory Cytokines in Antiarrhythmic Effects of Clofibrate in Ouabain-Induced Arrhythmia in Isolated Rat Atria.Advances in pharmacological sciences · 2016Article
- A compartmentalized mathematical model of the β1-adrenergic signaling system in mouse ventricular myocytes.PloS one · 2014Article
- Article
- Interpreting genetic effects through models of cardiac electromechanics.American journal of physiology. Heart and circulatory physiology · 2012Review
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Authors and funding
5 authors at 4 institutions in 2 countries.
Funding
Abstract
Transgenic mice overexpressing tumor necrosis factor-α (TNF-α mice) possess many of the features of human heart failure, such as dilated cardiomyopathy, impaired Ca(2+) handling, arrhythmias, and decreased survival. Although TNF-α mice have been studied extensively with a number of experimental methods, the mechanisms of heart failure are not completely understood. We created a mathematical model that reproduced experimentally observed changes in the action potential (AP) and Ca(2+) handling of isolated TNF-α mice ventricular myocytes. To study the contribution of the differences in ion currents, AP, Ca(2+) handling, and intercellular coupling to the development of arrhythmias in TNF-α mice, we further created several multicellular model tissues with combinations of wild-type (WT)/reduced gap junction conductance, WT/prolonged AP, and WT/decreased Na(+) current (I(Na)) amplitude. All model tissues were examined for susceptibility to Ca(2+) alternans, AP propagation block, and reentry. Our modeling results demonstrated that, similar to experimental data in TNF-α mice, Ca(2+) alternans in TNF-α tissues developed at longer basic cycle lengths. The greater susceptibility to Ca(2+) alternans was attributed to the prolonged AP, resulting in larger inactivation of I(Na), and to the decreased SR Ca(2+) uptake and corresponding smaller SR Ca(2+) load. Simulations demonstrated that AP prolongation induces an increased susceptibility to AP propagation block. Programmed stimulation of the model tissues with a premature impulse showed that reduced gap junction conduction increased the vulnerable window for initiation reentry, supporting the idea that reduced intercellular coupling is the major factor for reentrant arrhythmias in TNF-α mice.
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