Evidence map›Paper›PMID 31376190›Full record

ArticleBrain pathology (Zurich, Switzerland)2020

P2X7 activation enhances skeletal muscle metabolism and regeneration in SOD1G93A mouse model of amyotrophic lateral sclerosis.

Paola Fabbrizio, Savina Apolloni, Andrea Bianchi, Illari Salvatori, Cristiana Valle, Chiara Lanzuolo, Caterina Bendotti, Giovanni Nardo, Cinzia Volonté

Open access · hybridAbstract read
In one paragraph

Article in Brain pathology (Zurich, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

25 citing papers in PubMed, 38 citations in OpenAlex.

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  17. CaNeuroscience letters · 2021
    Review
  18. Where and Why Modeling Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2021
    Review
  19. Inflammasome in ALS Skeletal Muscle:International journal of molecular sciences · 2021
    Article
  20. Review
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

9 authors at 5 institutions in 2 countries.

Paola FabbrizioLaboratory of Molecular Neurobiology, Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy.
Savina ApolloniIRCCS Fondazione Santa Lucia, Rome, Italy.
Andrea BianchiIRCCS Fondazione Santa Lucia, Rome, Italy.
Illari SalvatoriIRCCS Fondazione Santa Lucia, Rome, Italy.
Cristiana ValleIRCCS Fondazione Santa Lucia, Rome, Italy.
Chiara LanzuoloIRCCS Fondazione Santa Lucia, Rome, Italy.
Caterina BendottiLaboratory of Molecular Neurobiology, Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy.
Giovanni NardoLaboratory of Molecular Neurobiology, Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milan, Italy.ORCID 0000-0002-1803-1484
Cinzia VolontéIRCCS Fondazione Santa Lucia, Rome, Italy.ORCID 0000-0001-7362-8307
Fondazione Santa Lucia · ITMario Negri Institute for Pharmacological Research · ITConstruction Technologies Institute · ITInstitute for Systems Analysis · RUIstituto di Farmacologia Traslazionale · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Muscle weakness plays an important role in neuromuscular disorders comprising amyotrophic lateral sclerosis (ALS). However, it is not established whether muscle denervation originates from the motor neurons, the muscles or more likely both. Previous studies have shown that the expression of the SOD1G93A mutation in skeletal muscles causes denervation of the neuromuscular junctions, inability to regenerate and consequent atrophy, all clear symptoms of ALS. In this work, we used SOD1G93A mice, a model that best mimics some pathological features of both familial and sporadic ALS, and we investigated some biological effects induced by the activation of the P2X7 receptor in the skeletal muscles. The P2X7, belonging to the ionotropic family of purinergic receptors for extracellular ATP, is abundantly expressed in the healthy skeletal muscles, where it controls cell duplication, differentiation, regeneration or death. In particular, we evaluated whether an in vivo treatment in SOD1G93A mice with the P2X7 specific agonist 2'(3')-O-(4-Benzoylbenzoyl) adenosine5'-triphosphate (BzATP) just before the onset of a pathological neuromuscular phenotype could exert beneficial effects in the skeletal muscles. Our findings indicate that stimulation of P2X7 improves the innervation and metabolism of myofibers, moreover elicits the proliferation/differentiation of satellite cells, thus preventing the denervation atrophy of skeletal muscles in SOD1G93A mice. Overall, this study suggests that a P2X7-targeted and site-specific modulation might be a strategy to interfere with the complex multifactorial and multisystem nature of ALS.

Indexed as

Amyotrophic Lateral SclerosisAnimalsDisease Models, AnimalMiceMice, TransgenicMuscle, SkeletalNeuromuscular JunctionReceptors, Purinergic P2X7RegenerationSuperoxide DismutaseP2rx7 protein, mouseReceptors, Purinergic P2X7SOD1 G93A proteinSuperoxide Dismutaseamyotrophic lateral sclerosispurinergic receptorsskeletal muscleSOD1G93A mice

Identifiers

PMID31376190
PMCPMC7065186
OpenAlexW2966489082

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.