Evidence map›Paper›PMID 23761627›Full record

ReviewAmerican journal of physiology. Cell physiology2013

Cellular mechanisms of tissue fibrosis. 4. Structural and functional consequences of skeletal muscle fibrosis.

Richard L Lieber, Samuel R Ward

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in American journal of physiology. Cell physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 188 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
188citing papers in PubMed, 3 pooled it
9.0field-weighted citation impact, top 1% 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

188 citing papers in PubMed, 3 syntheses or guidelines pooled it, 305 citations in OpenAlex.

  1. Pooled it
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  4. Trial
  5. AAV-mediated FGF21 gene therapy promotes health span extension by whole-body tissue-specific adaptations.Molecular therapy : the journal of the American Society of Gene Therapy · 2026
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128 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 1 institution in 1 country.

Richard L LieberDepartment of Orthopaedic Surgery, University of California San Diego, San Diego, California 92093-0863, USA. rlieber@ucsd.edu
Samuel R Ward
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
San Diego Skeletal Muscle Research CenterP30AR061303 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHEN, JU · 2011 to 2015
$3.3M
NIAMS NIH HHS P30 AR-061303NICHD NIH HHS R24 HD-050837
6 · The paper itself

Abstract

Skeletal muscle fibrosis can be a devastating clinical problem that arises from many causes, including primary skeletal muscle tissue diseases, as seen in the muscular dystrophies, or it can be secondary to events that include trauma to muscle or brain injury. The cellular source of activated fibroblasts (myofibroblasts) may include resident fibroblasts, adult muscle stem cells, or inflammatory or perivascular cells, depending on the model studied. Even though it is likely that there is no single source for all myofibroblasts, a common mechanism for the production of fibrosis is via the transforming growth factor-β/phosphorylated Smad3 pathway. This pathway and its downstream targets thus provide loci for antifibrotic therapies, as do methods for blocking the transdifferentiation of progenitors into activated fibroblasts. A structural model for the extracellular collagen network of skeletal muscle is needed so that measurements of collagen content, morphology, and gene expression can be related to mechanical properties. Approaches used to study fibrosis in tissues, such as lung, kidney, and liver, need to be applied to studies of skeletal muscle to identify ways to prevent or even cure the devastating maladies of skeletal muscle.

Indexed as

Muscle, SkeletalMyofibroblastsAnimalsCell TransdifferentiationCollagenExtracellular MatrixExtracellular Matrix ProteinsFibrosisHumansMuscular DiseasesMyostatinSmad3 ProteinTransforming Growth Factor betaWnt Signaling PathwayCollagenCTHRC1 protein, humanExtracellular Matrix ProteinsMSTN protein, humanMyostatinSmad3 ProteinSMAD3 protein, humanTransforming Growth Factor betamuscle mechanicsmyofibroblastpassive mechanicsstiffness

Identifiers

PMID23761627
PMCPMC3742845
OpenAlexW1965761285

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.