Evidence map›Paper›PMID 28709001›Full record

ArticleCell2017

Ciliary Hedgehog Signaling Restricts Injury-Induced Adipogenesis.

Daniel Kopinke, Elle C Roberson, Jeremy F Reiter

Open access · bronzeAbstract read
In one paragraph

Article in Cell, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 168 papers.

0numbers the graph read from it
0cells of the map it votes in
168citing papers in PubMed
8.5field-weighted citation impact, top 2% 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

168 citing papers in PubMed, 246 citations in OpenAlex.

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  16. Fibro-adipogenic progenitor cells from murine SMA muscles are intrinsically adipogenic.Proceedings of the National Academy of Sciences of the United States of America · 2026
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108 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Daniel KopinkeDepartment of Biochemistry and Biophysics, Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, USA.
Elle C RobersonDepartment of Biochemistry and Biophysics, Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, USA.
Jeremy F ReiterDepartment of Biochemistry and Biophysics, Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA, USA. Electronic address: jeremy.reiter@ucsf.edu.
University of California, San Francisco · US

Funding

GENETICS OF EUCARYOTIC AND PROCARYOTIC ORGANISMST32GM007810 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI ASHRAFI, KAVEH, NARLIKAR, GEETA J · 1985 to 2020
$15.1M
UCSF Nutrition Obesity Research CenterP30DK098722 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CHRISTIAN VAISSE · 2015 to 2026
$14.6M
Hedgehog signaling at the cell's antenna: Smoothened and the primary ciliumR01AR054396 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Jeremy F Reiter · 2007 to 2026
$9.0M
Obesity in Ciliopathies: How Neuronal Primary Cilia Control AppetiteR01DK106404 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI REITER, JEREMY F, VAISSE, CHRISTIAN · 2016 to 2025
$6.6M
Transition zone control of ciliary signalingR01GM095941 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI REITER, JEREMY F · 2011 to 2018
$3.4M
NIAMS NIH HHS R01 AR054396NIDDK NIH HHS P30 DK098722NIDDK NIH HHS R01 DK106404NIGMS NIH HHS R01 GM095941NIGMS NIH HHS T32 GM007810
6 · The paper itself

Abstract

Injured skeletal muscle regenerates, but with age or in muscular dystrophies, muscle is replaced by fat. Upon injury, muscle-resident fibro/adipogenic progenitors (FAPs) proliferated and gave rise to adipocytes. These FAPs dynamically produced primary cilia, structures that transduce intercellular cues such as Hedgehog (Hh) signals. Genetically removing cilia from FAPs inhibited intramuscular adipogenesis, both after injury and in a mouse model of Duchenne muscular dystrophy. Blocking FAP ciliation also enhanced myofiber regeneration after injury and reduced myofiber size decline in the muscular dystrophy model. Hh signaling through FAP cilia regulated the expression of TIMP3, a secreted metalloproteinase inhibitor, that inhibited MMP14 to block adipogenesis. A pharmacological mimetic of TIMP3 blocked the conversion of FAPs into adipocytes, pointing to a strategy to combat fatty degeneration of skeletal muscle. We conclude that ciliary Hh signaling by FAPs orchestrates the regenerative response to skeletal muscle injury.

Indexed as

AdipogenesisSignal TransductionAdipocytesAnimalsCiliaDystrophinHedgehog ProteinsMatrix Metalloproteinase 14MiceMuscle DevelopmentMuscle, SkeletalMuscular Dystrophy, DuchenneRegenerationStem CellsTissue Inhibitor of Metalloproteinase-3apo-dystrophin 1DystrophinHedgehog ProteinsMatrix Metalloproteinase 14Tissue Inhibitor of Metalloproteinase-3Duchenne muscular dystrophyfatty degenerationfibro/adipogenic progenitorsHedgehog signalingMMP14primary ciliumskeletal muscle regenerationTIMP3

Identifiers

PMID28709001
PMCPMC5617351
OpenAlexW2735513135

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.