Evidence map›Paper›PMID 39085209›Full record

ArticleNature communications2024

Serotonin reuptake inhibitors improve muscle stem cell function and muscle regeneration in male mice.

Mylène Fefeu, Michael Blatzer, Anita Kneppers, David Briand, Pierre Rocheteau, Alexandre Haroche, David Hardy, Mélanie Juchet-Martin, Anne Danckaert, François Coudoré and 7 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–field-weighted citation impact
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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. New insights into the skeletal muscle circadian clock in ruminants.Journal of animal science and biotechnology · 2026
    Review
  4. Article
  5. 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

17 authors.

Mylène FefeuGHU Paris Psychiatrie & Neurosciences, site Sainte Anne, Service Hospitalo-Universitaire de psychiatrie, Paris, France.
Michael BlatzerInstitut Pasteur, Experimental Neuropathology Unit, Global Health Department, Paris, France.
Anita Kneppers *Institut NeuroMyoGène, Unité Physiopathologie et Génétique du Neurone et du Muscle, Université Claude Bernard Lyon 1, CNRS UMR 5261, Inserm U1315, Univ Lyon, Lyon, France.ORCID 0000-0003-4901-5468
David Briand *Institut Pasteur, Experimental Neuropathology Unit, Global Health Department, Paris, France.ORCID 0000-0001-5680-8242
Pierre Rocheteau *Institut Pasteur, Experimental Neuropathology Unit, Global Health Department, Paris, France.
Alexandre HarocheGHU Paris Psychiatrie & Neurosciences, site Sainte Anne, Service Hospitalo-Universitaire de psychiatrie, Paris, France.
David HardyInstitut Pasteur, Experimental Neuropathology Unit, Global Health Department, Paris, France.ORCID 0000-0001-5874-4377
Mélanie Juchet-MartinInstitut Pasteur, Experimental Neuropathology Unit, Global Health Department, Paris, France.
Anne DanckaertInstitut Pasteur, UTechS PBI, C2RT, Paris, France.ORCID 0000-0001-8984-643X
François CoudoréCESP, MOODS Team, Inserm, Faculté de Pharmacie, Université Paris-Saclay, Châtenay-Malabry, France.
Abdulkarim TutakhailCESP, MOODS Team, Inserm, Faculté de Pharmacie, Université Paris-Saclay, Châtenay-Malabry, France.ORCID 0000-0002-4855-8084
Corinne HuchetTaRGeT, INSERM UMR 1089, Nantes Université, CHU Nantes, Nantes, France.
Aude LafouxTherassay Platform, Capacités, Université de Nantes, IRS 2 Nantes Biotech, Nantes, France.
Rémi MounierInstitut NeuroMyoGène, Unité Physiopathologie et Génétique du Neurone et du Muscle, Université Claude Bernard Lyon 1, CNRS UMR 5261, Inserm U1315, Univ Lyon, Lyon, France.
Olivier MirSarcoma Group, Gustave Roussy, Villejuif, France.
Raphaël GaillardGHU Paris Psychiatrie & Neurosciences, site Sainte Anne, Service Hospitalo-Universitaire de psychiatrie, Paris, France. raphael.gaillard@normalesup.org.
Fabrice ChrétienInstitut Pasteur, Experimental Neuropathology Unit, Global Health Department, Paris, France. f.chretien@ghu-paris.fr.ORCID 0000-0002-2794-1383

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Serotonin reuptake inhibitor antidepressants such as fluoxetine are widely used to treat mood disorders. The mechanisms of action include an increase in extracellular level of serotonin, neurogenesis, and growth of vessels in the brain. We investigated whether fluoxetine could have broader peripheral regenerative properties. Following prolonged administration of fluoxetine in male mice, we showed that fluoxetine increases the number of muscle stem cells and muscle angiogenesis, associated with positive changes in skeletal muscle function. Fluoxetine also improved skeletal muscle regeneration after single and multiples injuries with an increased muscle stem cells pool and vessel density associated with reduced fibrotic lesions and inflammation. Mice devoid of peripheral serotonin treated with fluoxetine did not exhibit beneficial effects during muscle regeneration. Specifically, pharmacological, and genetic inactivation of the 5-HT1B subtype serotonin receptor also abolished the enhanced regenerative process induced by fluoxetine. We highlight here a regenerative property of serotonin on skeletal muscle.

Indexed as

FluoxetineMuscle, SkeletalRegenerationSelective Serotonin Reuptake InhibitorsSerotoninAnimalsMaleMiceMice, Inbred C57BLNeovascularization, PhysiologicStem CellsFluoxetineSelective Serotonin Reuptake InhibitorsSerotonin

Identifiers

PMID39085209
PMCPMC11291725

What OpenQuestion holds

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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.