Evidence map›Paper›PMID 29408413›Full record

ReviewMatrix biology : journal of the International Society for Matrix Biology2018

Regulation of fibrosis in muscular dystrophy.

Lucas R Smith, Elisabeth R Barton

Open access · greenAbstract readReview
In one paragraph

Review in Matrix biology : journal of the International Society for Matrix Biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.

0numbers the graph read from it
0cells of the map it votes in
79citing papers in PubMed
4.7field-weighted citation impact, top 4% 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

79 citing papers in PubMed, 123 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Article
  9. Food science & nutrition · 2025
    Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. FAPs orchestrate homeostasis of muscle physiology and pathophysiology.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Review
  16. Article
  17. Article
  18. Zfp697 is an RNA-binding protein that regulates skeletal muscle inflammation and remodeling.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  19. Article
  20. Ablation of specific insulin-like growth factor I forms reveals the importance of cleavage for regenerative capacity and glycosylation for skeletal muscle storage.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article

19 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

Lucas R SmithDepartment of Chemical and Biomolecular Engineering, University of Pennsylvania, Philadelphia, PA, United States.
Elisabeth R BartonDepartment of Applied Physiology and Kinesiology, University of Florida, Gainesville, FL, United States. Electronic address: erbarton@ufl.edu.
University of Florida · USUniversity of Pennsylvania · US

Funding

Training and education CoreU54AR052646 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI MCNALLY, ELIZABETH M, SWEENEY, H LEE · 2005 to 2020
$24.1M
Modulation of Muscle Regenerationby Growth FactorsR01AR057363 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI BARTON, ELISABETH R · 2010 to 2014
$1.4M
The role of collagen organization in determination of fibrotic muscle function and regenerationK99AR067867 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI SMITH, LUCAS R · 2016 to 2017
$186k
NIAMS NIH HHS K99 AR067867NIAMS NIH HHS R01 AR057363NIAMS NIH HHS U54 AR052646
6 · The paper itself

Abstract

The production of force and power are inherent properties of skeletal muscle, and regulated by contractile proteins within muscle fibers. However, skeletal muscle integrity and function also require strong connections between muscle fibers and their extracellular matrix (ECM). A well-organized and pliant ECM is integral to muscle function and the ability for many different cell populations to efficiently migrate through ECM is critical during growth and regeneration. For many neuromuscular diseases, genetic mutations cause disruption of these cytoskeletal-ECM connections, resulting in muscle fragility and chronic injury. Ultimately, these changes shift the balance from myogenic pathways toward fibrogenic pathways, culminating in the loss of muscle fibers and their replacement with fatty-fibrotic matrix. Hence a common pathological hallmark of muscular dystrophy is prominent fibrosis. This review will cover the salient features of muscular dystrophy pathogenesis, highlight the signals and cells that are important for myogenic and fibrogenic actions, and discuss how fibrosis alters the ECM of skeletal muscle, and the consequences of fibrosis in developing therapies.

Indexed as

AnimalsClinical Trials as TopicExtracellular MatrixFibrosisHumansMuscle, SkeletalMuscular DystrophiesSignal TransductionMechanosensingMuscle regenerationSatellite cellsTransforming growth factor beta

Identifiers

PMID29408413
PMCPMC6519730
OpenAlexW2793221911

What OpenQuestion holds

Textmetadata
LicenceTDM
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.