Evidence map›Paper›PMID 27267062›Full record

ArticleCellular signalling2016

Fgf regulates dedifferentiation during skeletal muscle regeneration in adult zebrafish.

Alfonso Saera-Vila, Phillip E Kish, Alon Kahana

Abstract read
In one paragraph

Article in Cellular signalling, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.1field-weighted citation impact, top 15% 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

29 citing papers in PubMed, 45 citations in OpenAlex.

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  11. MAPK/ERK Pathway as a Central Regulator in Vertebrate Organ Regeneration.International journal of molecular sciences · 2022
    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

3 authors at 1 institution in 1 country.

Alfonso Saera-VilaDepartment of Ophthalmology and Visual Sciences, Kellogg Eye Center, University of Michigan, Ann Arbor, MI, USA.
Phillip E KishDepartment of Ophthalmology and Visual Sciences, Kellogg Eye Center, University of Michigan, Ann Arbor, MI, USA.
Alon KahanaDepartment of Ophthalmology and Visual Sciences, Kellogg Eye Center, University of Michigan, Ann Arbor, MI, USA. Electronic address: akahana@med.umich.edu.
University of Michigan · US

Funding

XenograftP30CA046592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI THEODORE S LAWRENCE · 1988 to 2026
$178.2M
Regional Pilot And Feasibility Study Grants ProgramP30DK020572 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Mehboob A Hussain · 2013 to 2026
$24.3M
ZEBRAFISH INTERNATIONAL RESOURCE CENTERP40RR012546 · NCRR · UNIVERSITY OF OREGON · PI WESTERFIELD, MONTE · 1998 to 2011
$21.9M
VIVARIUM MODULEP30EY007003 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI David Antonetti · 1987 to 2026
$17.6M
A Zebrafish model of extraocular muscle regeneration.R01EY022633 · NEI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI KAHANA, ALON · 2013 to 2016
$1.5M
NCI NIH HHS P30 CA046592NCRR NIH HHS P40 RR012546NEI NIH HHS P30 EY007003NEI NIH HHS R01 EY022633NIDDK NIH HHS P30 DK020572
6 · The paper itself

Abstract

Fibroblast growth factors (Fgfs) regulate critical biological processes such as embryonic development, tissue homeostasis, wound healing, and tissue regeneration. In zebrafish, Fgf signaling plays an important role in the regeneration of the spinal cord, liver, heart, fin, and photoreceptors, although its exact mechanism of action is not fully understood. Utilizing an adult zebrafish extraocular muscle (EOM) regeneration model, we demonstrate that blocking Fgf receptor function using either a chemical inhibitor (SU5402) or a dominant-negative transgenic construct (dnFGFR1a:EGFP) impairs muscle regeneration. Adult zebrafish EOMs regenerate through a myocyte dedifferentiation process, which involves a muscle-to-mesenchyme transition and cell cycle reentry by differentiated myocytes. Blocking Fgf signaling reduced cell proliferation and active caspase 3 levels in the regenerating muscle with no detectable levels of apoptosis, supporting the hypothesis that Fgf signaling is involved in the early steps of dedifferentiation. Fgf signaling in regenerating myocytes involves the MAPK/ERK pathway: inhibition of MEK activity with U0126 mimicked the phenotype of the Fgf receptor inhibition on both muscle regeneration and cell proliferation, and activated ERK (p-ERK) was detected in injured muscles by immunofluorescence and western blot. Interestingly, following injury, ERK2 expression is specifically induced and activated by phosphorylation, suggesting a key role in muscle regeneration. We conclude that the critical early steps of myocyte dedifferentiation in EOM regeneration are dependent on Fgf signaling.

Indexed as

Cell DedifferentiationRegenerationAgingAnimalsCell ProliferationFibroblast Growth FactorsGreen Fluorescent ProteinsMAP Kinase Signaling SystemModels, BiologicalMuscle, SkeletalOculomotor MusclesReceptor, Fibroblast Growth Factor, Type 1Zebrafishenhanced green fluorescent proteinFibroblast Growth FactorsGreen Fluorescent ProteinsReceptor, Fibroblast Growth Factor, Type 1Cell cycleCell reprogrammingHeat-shockMMTStrabismus

Identifiers

PMID27267062
PMCPMC4966975
OpenAlexW2415067433

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.