Evidence map›Paper›PMID 22442138›Full record

ArticleAmerican journal of physiology. Cell physiology2012

Skeletal muscle fibrosis develops in response to desmin deletion.

Gretchen A Meyer, Richard L Lieber

Abstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
2.7field-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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 63 citations in OpenAlex.

  1. Pooled it
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  9. Review
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  12. Article
  13. A unique sarcopenic progression in the mouse rotator cuff.Journal of cachexia, sarcopenia and muscle · 2022
    Article
  14. Article
  15. A mutation in desmin makes skeletal muscle less vulnerable to acute muscle damage after eccentric loading in rats.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021
    Article
  16. Article
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  19. Frontiers in genetics · 2021
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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

2 authors at 1 institution in 1 country.

Gretchen A MeyerDepartment of Bioengineering, University of California, San Diego, USA.
Richard L Lieber
University of California, San Diego · US

Funding

National Center for Muscle Rehabilitation ResearchR24HD050837 · NICHD · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LIEBER, RICHARD L., WARD, SAMUEL RICHARD · 2005 to 2014
$7.2M
Skeletal Muscle Injury: Mechanism Prevention &TreatmentR01AR040050 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI LIEBER, RICHARD L · 1989 to 2007
$1.6M
NIAMS NIH HHS AR-40050NICHD NIH HHS HD-050837NICHD NIH HHS R24 HD050837
6 · The paper itself

Abstract

Skeletal muscle is a dynamic composite of proteins that responds to both internal and external cues to facilitate muscle adaptation. In cases of disease or altered use, these messages can be distorted resulting in myopathic conditions such as fibrosis. In this work, we describe a mild and progressive fibrotic adaptation in skeletal muscle lacking the cytoskeletal intermediate filament protein desmin. Muscles lacking desmin become progressively stiffer, accumulate increased collagen, and increase expression of genes involved in extracellular matrix turnover. Additionally, in the absence of desmin, skeletal muscle is in an increased state of inflammation and regeneration as indicated by increased centrally nucleated fibers, elevated inflammation and regeneration related gene expression, and increased numbers of inflammatory cells. These data suggest a potential link between increased cellular damage and the development of fibrosis in muscles lacking the cytoskeletal support of the desmin filament network.

Indexed as

AnimalsDesminExtracellular MatrixFibrosisIntermediate FilamentsMiceMice, KnockoutMuscle Fibers, SkeletalMuscle, SkeletalMuscular DiseasesDesmin

Identifiers

PMID22442138
PMCPMC3378016
OpenAlexW2070482783

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.