Evidence map›Paper›PMID 31575088›Full record

ArticleCells2019

An Agonist of the CXCR4 Receptor Strongly Promotes Regeneration of Degenerated Motor Axon Terminals.

Samuele Negro, Giulia Zanetti, Andrea Mattarei, Alice Valentini, Aram Megighian, Giulia Tombesi, Alessandro Zugno, Valentina Dianin, Marco Pirazzini, Silvia Fillo and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cells, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 20% 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

17 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
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  8. Review
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  13. Motor function recovery: deciphering a regenerative niche at the neuromuscular synapse.Biological reviews of the Cambridge Philosophical Society · 2021
    Review
  14. Article
  15. Article
  16. Review
  17. A CXCR4 receptor agonist strongly stimulates axonal regeneration after damage.Annals of clinical and translational neurology · 2019
    Article
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

13 authors at 2 institutions in 1 country.

Samuele NegroDepartment of Biomedical Sciences, University of Padua, Padua 35131, Italy. samuele.negro1987@gmail.com.
Giulia ZanettiDepartment of Biomedical Sciences, University of Padua, Padua 35131, Italy. gzanetti89@gmail.com.
Andrea MattareiDepartment of Pharmaceutical and Pharmacological Sciences, University of Padua, Padua 35131, Italy. andrea.mattarei@unipd.it.
Alice ValentiniDepartment of Pharmaceutical and Pharmacological Sciences, University of Padua, Padua 35131, Italy. ali.valentini23@gmail.com.
Aram MegighianDepartment of Biomedical Sciences, University of Padua, Padua 35131, Italy. aram.megighian@gmail.com.
Giulia TombesiDepartment of Biology, University of Padua, Padua 35131, Italy. giulia.tombesi@phd.unipd.it.
Alessandro ZugnoDepartment of Pharmaceutical and Pharmacological Sciences, University of Padua, Padua 35131, Italy. alessandro.zugno@phd.unipd.it.
Valentina DianinDepartment of Pharmaceutical and Pharmacological Sciences, University of Padua, Padua 35131, Italy. valedianin@gmail.com.
Marco PirazziniDepartment of Biomedical Sciences, University of Padua, Padua 35131, Italy. marcopiraz@gmail.com.
Silvia FilloCenter of Medical and Veterinary Research of the Ministry of Defence, Rome 00184, Italy. silviafillo@gmail.com.
Florigio ListaCenter of Medical and Veterinary Research of the Ministry of Defence, Rome 00184, Italy. romano.lista@gmail.com.
Michela RigoniDepartment of Biomedical Sciences, University of Padua, Padua 35131, Italy. rigonimic@gmail.com.
Cesare MontecuccoDepartment of Biomedical Sciences, University of Padua, Padua 35131, Italy. cesare.montecucco@gmail.com.
University of Padua · ITMinistry of Defence · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The activation of the G-protein coupled receptor CXCR4 by its ligand CXCL12α is involved in a large variety of physiological and pathological processes, including the growth of B cells precursors and of motor axons, autoimmune diseases, stem cell migration, inflammation, and several neurodegenerative conditions. Recently, we demonstrated that CXCL12α potently stimulates the functional recovery of damaged neuromuscular junctions via interaction with CXCR4. This result prompted us to test the neuroregeneration activity of small molecules acting as CXCR4 agonists, endowed with better pharmacokinetics with respect to the natural ligand. We focused on NUCC-390, recently shown to activate CXCR4 in a cellular system. We designed a novel and convenient chemical synthesis of NUCC-390, which is reported here. NUCC-390 was tested for its capability to induce the regeneration of motor axon terminals completely degenerated by the presynaptic neurotoxin α-Latrotoxin. NUCC-390 was found to strongly promote the functional recovery of the neuromuscular junction, as assayed by electrophysiology and imaging. This action is CXCR4 dependent, as it is completely prevented by AMD3100, a well-characterized CXCR4 antagonist. These data make NUCC-390 a strong candidate to be tested in human therapy to promote nerve recovery of function after different forms of neurodegeneration.

Indexed as

AnimalsBenzylaminesCyclamsHeterocyclic CompoundsIndazolesMiceMice, Inbred StrainsMotor NeuronsNerve DegenerationNerve RegenerationNeuromuscular JunctionPiperidinesPresynaptic TerminalsPrimary Cell CulturePyridinesRatsalpha-latrotoxinBenzylaminesCyclamsHeterocyclic CompoundsIndazolesNUCC-390PiperidinesplerixaforPyridinesReceptors, CXCR4Spider VenomsCXCR4 receptormotor neuronneurodegenerationneuromuscular junctionneuroregeneration

Identifiers

PMID31575088
PMCPMC6829515
OpenAlexW2976922937

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.