Evidence map›Paper›PMID 22589710›Full record

ArticlePLoS computational biology2012

Filament compliance influences cooperative activation of thin filaments and the dynamics of force production in skeletal muscle.

Bertrand C W Tanner, Thomas L Daniel, Michael Regnier

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.1field-weighted citation impact, top 12% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

46 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
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  4. Modeling cardiac contractile cooperativity across species.The Journal of general physiology · 2025
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  11. Effect of Myosin Isoforms on Cardiac Muscle Twitch of Mice, Rats and Humans.International journal of molecular sciences · 2022
    Article
  12. Article
  13. Hypertrophic cardiomyopathy β-cardiac myosin mutation (P710R) leads to hypercontractility by disrupting super relaxed state.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  14. Article
  15. Article
  16. Mavacamten decreases maximal force and CaAmerican journal of physiology. Heart and circulatory physiology · 2021
    Article
  17. Article
  18. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 2 institutions in 1 country.

Bertrand C W TannerDepartment of Molecular Physiology and Biophysics, University of Vermont, Burlington, Vermont, United States of America. btanner@uvm.edu
Thomas L Daniel
Michael Regnier
University of Washington · USUniversity of Vermont · US

Funding

COOPERATIVE THIN FILAMENT ACTIVATION IN STRIATED MUSCLER01HL065497 · NHLBI · UNIVERSITY OF WASHINGTON · PI REGNIER, MICHAEL · 2001 to 2012
$4.5M
Bioengineering Cardiovascular Training GrantT32EB001650 · NIBIB · UNIVERSITY OF WASHINGTON · PI REGNIER, MICHAEL · 2004 to 2019
$3.6M
NHLBI NIH HHS HL65497NHLBI NIH HHS R01 HL065497NIBIB NIH HHS T32 EB001650
6 · The paper itself

Abstract

Striated muscle contraction is a highly cooperative process initiated by Ca²⁺ binding to the troponin complex, which leads to tropomyosin movement and myosin cross-bridge (XB) formation along thin filaments. Experimental and computational studies suggest skeletal muscle fiber activation is greatly augmented by cooperative interactions between neighboring thin filament regulatory units (RU-RU cooperativity; 1 RU = 7 actin monomers+1 troponin complex+1 tropomyosin molecule). XB binding can also amplify thin filament activation through interactions with RUs (XB-RU cooperativity). Because these interactions occur with a temporal order, they can be considered kinetic forms of cooperativity. Our previous spatially-explicit models illustrated that mechanical forms of cooperativity also exist, arising from XB-induced XB binding (XB-XB cooperativity). These mechanical and kinetic forms of cooperativity are likely coordinated during muscle contraction, but the relative contribution from each of these mechanisms is difficult to separate experimentally. To investigate these contributions we built a multi-filament model of the half sarcomere, allowing RU activation kinetics to vary with the state of neighboring RUs or XBs. Simulations suggest Ca²⁺ binding to troponin activates a thin filament distance spanning 9 to 11 actins and coupled RU-RU interactions dominate the cooperative force response in skeletal muscle, consistent with measurements from rabbit psoas fibers. XB binding was critical for stabilizing thin filament activation, particularly at submaximal Ca²⁺ levels, even though XB-RU cooperativity amplified force less than RU-RU cooperativity. Similar to previous studies, XB-XB cooperativity scaled inversely with lattice stiffness, leading to slower rates of force development as stiffness decreased. Including RU-RU and XB-RU cooperativity in this model resulted in the novel prediction that the force-[Ca²⁺] relationship can vary due to filament and XB compliance. Simulations also suggest kinetic forms of cooperativity occur rapidly and dominate early to get activation, while mechanical forms of cooperativity act more slowly, augmenting XB binding as force continues to develop.

Indexed as

Models, BiologicalActin CytoskeletonAnimalsCalciumCalcium SignalingComputer SimulationHumansMolecular Motor ProteinsMuscle ContractionMuscle, SkeletalSarcomeresStress, MechanicalCalciumMolecular Motor Proteins

Identifiers

PMID22589710
PMCPMC3349719
OpenAlexW2038891601

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.