ArticleBiophysical journal2010
Coupling of adjacent tropomyosins enhances cross-bridge-mediated cooperative activation in a markov model of the cardiac thin filament.
Article in Biophysical journal, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed.
- Modeling cardiac contractile cooperativity across species.The Journal of general physiology · 2025Article
- Modeling the effects of thin filament near-neighbor cooperative interactions in mammalian myocardium.The Journal of general physiology · 2025Article
- Mechanistic insights into effects of the cardiac myosin activator omecamtiv mecarbil from mechanokinetic modelling.Frontiers in physiology · 2025Article
- Cardiac length-dependent activation driven by force-dependent thick-filament dynamics.Biophysical journal · 2024Article
- Multiscale modeling shows how 2'-deoxy-ATP rescues ventricular function in heart failure.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Harnessing molecular mechanism for precision medicine in dilated cardiomyopathy caused by a mutation in troponin T.bioRxiv : the preprint server for biology · 2024Article
- Proposing a Caputo-Land System for active tension. Capturing variable viscoelasticity.Heliyon · 2024Article
- Design Principles and Benefits of Spatially Explicit Models of Myofilament Function.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Muscle LIM Protein Force-Sensing Mediates Sarcomeric Biomechanical Signaling in Human Familial Hypertrophic Cardiomyopathy.Circulation · 2022Article
- Heart-on-Chip for Combined Cellular Dynamics Measurements and Computational Modeling Towards Clinical Applications.Annals of biomedical engineering · 2022Review
- A NovelFrontiers in physiology · 2022Article
- Cardiac myosin contraction and mechanotransduction in health and disease.The Journal of biological chemistry · 2021Review
- A mathematical model of hiPSC cardiomyocytes electromechanics.Physiological reports · 2021Article
- Loss of crossbridge inhibition drives pathological cardiac hypertrophy in patients harboring the TPM1 E192K mutation.The Journal of general physiology · 2021Article
- Potential impacts of the cardiac troponin I mobile domain on myofilament activation and relaxation.Journal of molecular and cellular cardiology · 2021Article
- Mechanical dysfunction of the sarcomere induced by a pathogenic mutation in troponin T drives cellular adaptation.The Journal of general physiology · 2021Article
- Biophysically detailed mathematical models of multiscale cardiac active mechanics.PLoS computational biology · 2020Article
- Cardiac muscle regulatory units are predicted to interact stronger than neighboring cross-bridges.Scientific reports · 2020Article
- Variant R94C inJournal of the American Heart Association · 2020Article
- A Dynamic Situation with Uncertainty: Multiscale Modeling of Cardiac Thin-Filament CaBiophysical journal · 2019Article
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4 authors.
Funding
Abstract
We developed a Markov model of cardiac thin filament activation that accounts for interactions among nearest-neighbor regulatory units (RUs) in a spatially explicit manner. Interactions were assumed to arise from structural coupling of adjacent tropomyosins (Tms), such that Tm shifting within each RU was influenced by the Tm status of its neighbors. Simulations using the model demonstrate that this coupling is sufficient to produce observed cooperativity in both steady-state and dynamic force-Ca(2+) relationships. The model was further validated by comparison with reported responses under various conditions including inhibition of myosin binding and the addition of strong-binding, non-force-producing myosin fragments. The model also reproduced the effects of 2.5 mM added P(i) on Ca(2+)-activated force and the rate of force redevelopment measured in skinned rat myocardial preparations. Model analysis suggests that Tm-Tm coupling potentiates the activating effects of strongly-bound cross-bridges and contributes to force-Ca(2+) dynamics of intact cardiac muscle. The model further predicts that activation at low Ca(2+) concentrations is cooperatively inhibited by nearest neighbors, requiring Ca(2+) binding to >25% of RUs to produce appreciable levels of force. Without excluding other putative cooperative mechanisms, these findings suggest that structural coupling of adjacent Tm molecules contributes to several properties of cardiac myofilament activation.
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