Evidence map›Paper›PMID 36970609›Full record

ArticleMatrix biology plus2023

The extracellular matrix of dystrophic mouse diaphragm accounts for the majority of its passive stiffness and is resistant to collagenase digestion.

Ross P Wohlgemuth, Ryan M Feitzinger, Kyle E Henricson, Daryl T Dinh, Sarah E Brashear, Lucas R Smith

Open access · goldAbstract read
In one paragraph

Article in Matrix biology plus, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

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

6 authors at 2 institutions in 1 country.

Ross P WohlgemuthDepartment of Neurobiology, Physiology, and Behavior, University of California Davis, USA.
Ryan M FeitzingerDepartment of Neurobiology, Physiology, and Behavior, University of California Davis, USA.
Kyle E HenricsonDepartment of Neurobiology, Physiology, and Behavior, University of California Davis, USA.
Daryl T DinhDepartment of Neurobiology, Physiology, and Behavior, University of California Davis, USA.
Sarah E BrashearDepartment of Neurobiology, Physiology, and Behavior, University of California Davis, USA.
Lucas R SmithDepartment of Neurobiology, Physiology, and Behavior, University of California Davis, USA.
University of California, Davis · USUniversity of California, Santa Cruz · US

Funding

Interdependency of fibroadipogenic progenitors and extracellular matrix that drive skeletal muscle fibrosisR01AR079545 · NIAMS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI LUCAS R SMITH · 2022 to 2026
$2.5M
NIAMS NIH HHS R01 AR079545
6 · The paper itself

Abstract

The healthy skeletal muscle extracellular matrix (ECM) has several functions including providing structural integrity to myofibers, enabling lateral force transmission, and contributing to overall passive mechanical properties. In diseases such as Duchenne Muscular dystrophy, there is accumulation of ECM materials, primarily collagen, which results in fibrosis. Previous studies have shown that fibrotic muscle is often stiffer than healthy muscle, in part due to the increased number and altered architecture of collagen fibers within the ECM. This would imply that the fibrotic matrix is stiffer than the healthy matrix. However, while previous studies have attempted to quantify the extracellular contribution to passive stiffness in muscle, the outcomes are dependent on the type of method used. Thus, the goals of this study were to compare the stiffness of healthy and fibrotic muscle ECM and to demonstrate the efficacy of two methods for quantifying extracellular-based stiffness in muscle, namely decellularization and collagenase digestion. These methods have been demonstrated to remove the muscle fibers or ablate collagen fiber integrity, respectively, while maintaining the contents of the extracellular matrix. Using these methods in conjunction with mechanical testing on wildtype and D2.

Indexed as

CollagenaseDecellularizationFibrosisMuscular DystrophySkeletal Muscle Mechanics

Identifiers

PMID36970609
PMCPMC10036937
OpenAlexW4324029731

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.