Evidence map›Paper›PMID 25844152›Full record

ArticleInterface focus2015

Multiscale models of skeletal muscle reveal the complex effects of muscular dystrophy on tissue mechanics and damage susceptibility.

Kelley M Virgilio, Kyle S Martin, Shayn M Peirce, Silvia S Blemker

Open access · bronzeAbstract read
In one paragraph

Article in Interface focus, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 79 citations in OpenAlex.

  1. Article
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  6. Review
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  9. Article
  10. Role of Muscle LIM Protein in Mechanotransduction Process.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. MRI and muscle imaging for idiopathic inflammatory myopathies.Brain pathology (Zurich, Switzerland) · 2021
    Review
  16. Article
  17. Review
  18. Article
  19. TowardsFrontiers in bioengineering and biotechnology · 2021
    Review
  20. Multi-scale models of lung fibrosis.Matrix biology : journal of the International Society for Matrix Biology · 2020
    Review
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

4 authors at 1 institution in 1 country.

Kelley M VirgilioDepartment of Biomedical Engineering , University of Virginia , Charlottesville, VA 22908 , USA.
Kyle S MartinDepartment of Biomedical Engineering , University of Virginia , Charlottesville, VA 22908 , USA.
Shayn M PeirceDepartment of Biomedical Engineering , University of Virginia , Charlottesville, VA 22908 , USA.
Silvia S BlemkerDepartment of Biomedical Engineering , University of Virginia , Charlottesville, VA 22908 , USA ; Department of Orthopaedic Surgery , University of Virginia , Charlottesville, VA 22908 , USA ; Department of Mechanical and Aerospace Engineering , University of Virginia , Charlottesville, VA 22908 , USA.
University of Virginia · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Computational models have been increasingly used to study the tissue-level constitutive properties of muscle microstructure; however, these models were not created to study or incorporate the influence of disease-associated modifications in muscle. The purpose of this paper was to develop a novel multiscale muscle modelling framework to elucidate the relationship between microstructural disease adaptations and modifications in both mechanical properties of muscle and strain in the cell membrane. We used an agent-based model to randomly generate new muscle fibre geometries and mapped them into a finite-element model representing a cross section of a muscle fascicle. The framework enabled us to explore variability in the shape and arrangement of fibres, as well as to incorporate disease-related changes. We applied this method to reveal the trade-offs between mechanical properties and damage susceptibility in Duchenne muscular dystrophy (DMD). DMD is a fatal genetic disease caused by a lack of the transmembrane protein dystrophin, leading to muscle wasting and death due to cardiac or pulmonary complications. The most prevalent microstructural variations in DMD include: lack of transmembrane proteins, fibrosis, fatty infiltration and variation in fibre cross-sectional area. A parameter analysis of these variations and case study of DMD revealed that the nature of fibrosis and density of transmembrane proteins strongly affected the stiffness of the muscle and susceptibility to membrane damage.

Indexed as

agent-basedfibrosismicromechanicalmultiscalemusclemuscular dystrophy

Identifiers

PMID25844152
PMCPMC4342948
OpenAlexW2112589767

What OpenQuestion holds

Textmetadata
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.