ArticleProceedings of the National Academy of Sciences of the United States of America2016
Size and speed of the working stroke of cardiac myosin in situ.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 51 citations in OpenAlex.
- Theoretical treatment of tension transients in muscle following sudden changes in orthophosphate concentration: implications for energy transduction.Journal of muscle research and cell motility · 2025Article
- The elementary step that generates force and sinusoidal analysis in striated muscle fibers.Journal of muscle research and cell motility · 2025Review
- Functional control of myosin motors in the cardiac cycle.Nature reviews. Cardiology · 2025Review
- An integrated picture of the structural pathways controlling the heart performance.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Single-Molecule Investigation of Load-Dependent Actomyosin Dissociation Kinetics for Cardiac and Slow Skeletal Myosin.Small (Weinheim an der Bergstrasse, Germany) · 2024Article
- Cardiac ventricular myosin and slow skeletal myosin exhibit dissimilar chemomechanical properties despite bearing the same myosin heavy chain isoform.The Journal of biological chemistry · 2022Article
- Effect of Myosin Isoforms on Cardiac Muscle Twitch of Mice, Rats and Humans.International journal of molecular sciences · 2022Article
- The regulatory light chain mediates inactivation of myosin motors during active shortening of cardiac muscle.Nature communications · 2021Article
- The Synergic Role of Actomyosin Architecture and Biased Detachment in Muscle Energetics: Insights in Cross Bridge Mechanism Beyond the Lever-Arm Swing.International journal of molecular sciences · 2021Article
- A reverse stroke characterizes the force generation of cardiac myofilaments, leading to an understanding of heart function.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The effect of variable troponin C mutation thin filament incorporation on cardiac muscle twitch contractions.Journal of molecular and cellular cardiology · 2021Article
- Multiscale modeling of twitch contractions in cardiac trabeculae.The Journal of general physiology · 2021Article
- Active Force Generation in Cardiac Muscle Cells: Mathematical Modeling and Numerical Simulation of the Actin-Myosin Interaction.Vietnam journal of mathematics · 2021Review
- Biophysically detailed mathematical models of multiscale cardiac active mechanics.PLoS computational biology · 2020Article
- Orthophosphate increases the efficiency of slow muscle-myosin isoform in the presence of omecamtiv mecarbil.Nature communications · 2020Article
- Dobutamine stress testing in patients with Fontan circulation augmented by biomechanical modeling.PloS one · 2020Article
- Article
- The Mechanical Power of Titin Folding.Cell reports · 2019Article
- How myofilament strain and strain rate lead the dance of the cardiac cycle.Archives of biochemistry and biophysics · 2019Review
- Proposed mechanism for the length dependence of the force developed in maximally activated muscles.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The power in the myocardium sarcomere is generated by two bipolar arrays of the motor protein cardiac myosin II extending from the thick filament and pulling the thin, actin-containing filaments from the opposite sides of the sarcomere. Despite the interest in the definition of myosin-based cardiomyopathies, no study has yet been able to determine the mechanokinetic properties of this motor protein in situ. Sarcomere-level mechanics recorded by a striation follower is used in electrically stimulated intact ventricular trabeculae from the rat heart to determine the isotonic velocity transient following a stepwise reduction in force from the isometric peak force TP to a value T(0.8-0.2 TP). The size and the speed of the early rapid shortening (the isotonic working stroke) increase by reducing T from ∼3 nm per half-sarcomere (hs) and 1,000 s(-1) at high load to ∼8 nm⋅hs(-1) and 6,000 s(-1) at low load. Increases in sarcomere length (1.9-2.2 μm) and external [Ca(2+)]o (1-2.5 mM), which produce an increase of TP, do not affect the dependence on T, normalized for TP, of the size and speed of the working stroke. Thus, length- and Ca(2+)-dependent increase of TP and power in the heart can solely be explained by modulation of the number of myosin motors, an emergent property of their array arrangement. The motor working stroke is similar to that of skeletal muscle myosin, whereas its speed is about three times slower. A new powerful tool for investigations and therapies of myosin-based cardiomyopathies is now within our reach.
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