Evidence map›Paper›PMID 25766255›Full record

ArticleThe EMBO journal2015

FGF22 signaling regulates synapse formation during post-injury remodeling of the spinal cord.

Anne Jacobi, Kristina Loy, Anja M Schmalz, Mikael Hellsten, Hisashi Umemori, Martin Kerschensteiner, Florence M Bareyre

Open access · greenAbstract read
In one paragraph

Article in The EMBO journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

33 citing papers in PubMed, 50 citations in OpenAlex.

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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

7 authors at 3 institutions in 2 countries.

Anne JacobiInstitute of Clinical Neuroimmunology, Ludwig-Maximilians Universität München, Munich, Germany.
Kristina LoyInstitute of Clinical Neuroimmunology, Ludwig-Maximilians Universität München, Munich, Germany.
Anja M SchmalzInstitute of Clinical Neuroimmunology, Ludwig-Maximilians Universität München, Munich, Germany.
Mikael HellstenInstitute of Clinical Neuroimmunology, Ludwig-Maximilians Universität München, Munich, Germany.
Hisashi UmemoriDepartment of Neurology, F.M. Kirby Neurobiology Center, Boston Children's Hospital, Harvard Medical School, Boston, MA, USA Molecular & Behavioral Neuroscience Institute and Department of Biological Chemistry, University of Michigan Medical School, Ann Arbor, MI, USA.
Martin KerschensteinerInstitute of Clinical Neuroimmunology, Ludwig-Maximilians Universität München, Munich, Germany Munich Cluster of Systems Neurology (SyNergy), Munich, Germany.
Florence M BareyreInstitute of Clinical Neuroimmunology, Ludwig-Maximilians Universität München, Munich, Germany Munich Cluster of Systems Neurology (SyNergy), Munich, Germany Florence.Bareyre@med.uni-muenchen.de.
Ludwig-Maximilians-Universität München · DEMunich Cluster for Systems Neurology · DEBoston Children's Hospital · US

Funding

SYNAPTIC MECHANISMS IN HIPPOCAMPAL EPILEPTOGENESISP30HD018655 · NICHD · CHILDREN'S HOSPITAL BOSTON · PI CHEN, CHINFEI · 1985 to 2015
$26.2M
Excitatory and inhibitory synaptogenesis by FGFs and their role in epilepsyR01NS070005 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI UMEMORI, HISASHI · 2010 to 2014
$1.6M
NICHD NIH HHS P30 HD018655NINDS NIH HHS NS070005NINDS NIH HHS R01 NS070005
6 · The paper itself

Abstract

The remodeling of axonal circuits after injury requires the formation of new synaptic contacts to enable functional recovery. Which molecular signals initiate such axonal and synaptic reorganisation in the adult central nervous system is currently unknown. Here, we identify FGF22 as a key regulator of circuit remodeling in the injured spinal cord. We show that FGF22 is produced by spinal relay neurons, while its main receptors FGFR1 and FGFR2 are expressed by cortical projection neurons. FGF22 deficiency or the targeted deletion of FGFR1 and FGFR2 in the hindlimb motor cortex limits the formation of new synapses between corticospinal collaterals and relay neurons, delays their molecular maturation, and impedes functional recovery in a mouse model of spinal cord injury. These results establish FGF22 as a synaptogenic mediator in the adult nervous system and a crucial regulator of synapse formation and maturation during post-injury remodeling in the spinal cord.

Indexed as

AnimalsAxonsFibroblast Growth FactorsMice, Inbred C57BLMice, KnockoutNerve RegenerationNeuronal PlasticityNeuronsReceptor, Fibroblast Growth Factor, Type 1Receptor, Fibroblast Growth Factor, Type 2Signal TransductionSpinal Cord InjuriesSynapsesFgf22 protein, mouseFgfr1 protein, mouseFgfr2 protein, mouseFibroblast Growth FactorsReceptor, Fibroblast Growth Factor, Type 1Receptor, Fibroblast Growth Factor, Type 2axonal remodelingfibroblast growth factorfunctional recoveryspinal cord injurysynapse formation

Identifiers

PMID25766255
PMCPMC4426482
OpenAlexW2020193978

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.