Evidence map›Paper›PMID 26616495›Full record

ArticleMuscle & nerve2016

Increased collagen cross-linking is a signature of dystrophin-deficient muscle.

Lucas R Smith, David W Hammers, H Lee Sweeney, Elisabeth R Barton

Open access · hybridAbstract read
In one paragraph

Article in Muscle & nerve, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.

0numbers the graph read from it
0cells of the map it votes in
63citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

63 citing papers in PubMed, 87 citations in OpenAlex.

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  16. Thrown for a loop: fibro-adipogenic progenitors in skeletal muscle fibrosis.American journal of physiology. Cell physiology · 2023
    Review
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3 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

4 authors at 1 institution in 1 country.

Lucas R SmithDepartment of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
David W HammersDepartment of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
H Lee SweeneyDepartment of Physiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
Elisabeth R BartonPennsylvania Muscle Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
University of Pennsylvania · US

Funding

Training and education CoreU54AR052646 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI MCNALLY, ELIZABETH M, SWEENEY, H LEE · 2005 to 2020
$24.1M
Training in Muscle Biology and Muscle DiseaseT32AR053461 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI OSTAP, E. MICHAEL · 2006 to 2025
$4.9M
Modulation of Muscle Regenerationby Growth FactorsR01AR057363 · NIAMS · UNIVERSITY OF PENNSYLVANIA · PI BARTON, ELISABETH R · 2010 to 2014
$1.4M
NIAMS NIH HHS R01 AR057363NIAMS NIH HHS T32 AR053461NIAMS NIH HHS U54 AR052646
6 · The paper itself

Abstract

introductionCollagen cross-linking is a key parameter in extracellular matrix (ECM) maturation, turnover, and stiffness. We examined aspects of collagen cross-linking in dystrophin-deficient murine, canine, and human skeletal muscle.

methodsDMD patient biopsies and samples from mdx mice and golden retriever muscular dystrophy dog samples (with appropriate controls) were analyzed. Collagen cross-linking was evaluated using solubility and hydroxyproline assays. Expression of the cross-linking enzyme lysyl oxidase (LOX) was determined by real-time polymerase chain reaction, immunoblotting, and immunofluorescence.

resultsLOX protein levels are increased in dystrophic muscle from all species evaluated. Dystrophic mice and dogs had significantly higher cross-linked collagen than controls, especially in the diaphragm. Distribution of intramuscular LOX was heterogeneous in all samples, but it increased in frequency and intensity in dystrophic muscle.

conclusionThese findings implicate elevated collagen cross-linking as an important component of the disrupted ECM in dystrophic muscles, and heightened cross-linking is evident in mouse, dog, and man. Muscle Nerve 54: 71-78, 2016.

Indexed as

AdolescentAnimalsChildCollagenDiaphragmDogsFemaleHumansHydroxyprolineMaleMiceMice, Inbred C57BLMice, Inbred mdxMuscle, SkeletalMuscular Dystrophy, DuchenneProtein-Lysine 6-OxidaseCollagenHydroxyprolineProtein-Lysine 6-OxidaseRNA, MessengerVimentincollagen cross-linkingextracellular matrixfibrosislysyl oxidasemuscular dystrophy

Identifiers

PMID26616495
PMCPMC5067682
OpenAlexW2179408168

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.