Evidence map›Paper›PMID 37820010›Full record

ArticleScience translational medicine2023

Regeneration of neuromuscular synapses after acute and chronic denervation by inhibiting the gerozyme 15-prostaglandin dehydrogenase.

Mohsen A Bakooshli, Yu Xin Wang, Elena Monti, Shiqi Su, Peggy Kraft, Minas Nalbandian, Ludmila Alexandrova, Joshua R Wheeler, Hannes Vogel, Helen M Blau

Open access · greenAbstract read
In one paragraph

Article in Science translational medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

38 citing papers in PubMed, 37 citations in OpenAlex.

  1. Targeting prostaglandin catabolism via topical nanotherapy rescues vision in ischemic optic neuropathy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. 15-PGDH inhibition promotes muscle repair and strength recovery during GLP-1 receptor agonist-induced weight loss.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  7. Junctions in Jeopardy: the neuromuscular junction is a selective pathological target in Charcot-Marie-Tooth disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    Review
  8. Review
  9. Article
  10. Article
  11. Molecular evolution of animal aging.The EMBO journal · 2026
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. Article
  19. Review
  20. The multimodal transcriptional response of denervated skeletal muscle involves regulation ofProceedings of the National Academy of Sciences of the United States of America · 2025
    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

10 authors at 2 institutions in 1 country.

Mohsen A BakooshliBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0002-3577-3332
Yu Xin WangBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0001-8440-9388
Elena MontiBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0002-3767-0855
Shiqi SuBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0001-7812-2081
Peggy KraftBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.
Minas NalbandianBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0002-1018-3483
Ludmila AlexandrovaVincent Coates Foundation Mass Spectrometry Laboratory, Stanford University, Stanford, CA 94305, USA.ORCID 0000-0002-1203-4166
Joshua R WheelerDepartment of Pathology, Stanford University, Stanford, CA 94305, USA.
Hannes VogelDepartment of Pathology, Stanford University, Stanford, CA 94305, USA.ORCID 0000-0002-0960-3508
Helen M BlauBaxter Laboratory for Stem Cell Biology, Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA.ORCID 0000-0001-6503-5480
Stanford University · USDiscovery Institute · US

Funding

Stem Cells for Brain and BrawnR01AG020961 · NIA · STANFORD UNIVERSITY · PI BLAU, HELEN M · 2002 to 2019
$5.0M
Regulation of eicosanoid signaling lipids to improve skeletal muscle function and increase healthspan during agingR01AG069858 · NIA · STANFORD UNIVERSITY · PI BLAU, HELEN M · 2020 to 2023
$2.4M
Learning Regulatory Drivers of Chromatin and Expression Dynamics during Nuclear ReprogrammingR01HG009674 · NHGRI · STANFORD UNIVERSITY · PI BLAU, HELEN M, KUNDAJE, ANSHUL · 2017 to 2019
$2.1M
Spatial Regulators of Skeletal Muscle Regeneration and DiseaseR00NS120278 · NINDS · SANFORD BURNHAM PREBYS MEDICAL DISCOVERY INSTITUTE · PI WANG, YU XIN · 2023 to 2025
$739k
Xevo TQ-XS Triple Quadrupole Mass Spectrometer SystemS10OD026962 · OD · STANFORD UNIVERSITY · PI CHIEN, ALLIS SOE-LANG · 2019 to 2019
$527k
Spatial Regulators of Skeletal Muscle Regeneration and DiseaseK99NS120278 · NINDS · STANFORD UNIVERSITY · PI WANG, YU XIN · 2020 to 2021
$177k
NHGRI NIH HHS R01 HG009674NIA NIH HHS R01 AG020961NIA NIH HHS R01 AG069858NIH HHS S10 OD026962NINDS NIH HHS K99 NS120278NINDS NIH HHS R00 NS120278
6 · The paper itself

Abstract

To date, there are no approved treatments for the diminished strength and paralysis that result from the loss of peripheral nerve function due to trauma, heritable neuromuscular diseases, or aging. Here, we showed that denervation resulting from transection of the sciatic nerve triggered a marked increase in the prostaglandin-degrading enzyme 15-hydroxyprostaglandin dehydrogenase (15-PGDH) in skeletal muscle in mice, providing evidence that injury drives early expression of this aging-associated enzyme or gerozyme. Treating mice with a small-molecule inhibitor of 15-PGDH promoted regeneration of motor axons and formation of neuromuscular synapses leading to an acceleration in recovery of force after an acute nerve crush injury. In aged mice with chronic denervation of muscles, treatment with the 15-PGDH inhibitor increased motor neuron viability and restored neuromuscular junctions and function. These presynaptic changes synergized with previously reported muscle tissue remodeling to result in a marked increase in the strength of aged muscles. We further found that 15-PGDH aggregates defined the target fibers that are histopathologic hallmarks of human neurogenic myopathies, suggesting that the gerozyme may be involved in their etiology. Our data suggest that inhibition of 15-PGDH may constitute a therapeutic strategy to physiologically boost prostaglandin E2, restore neuromuscular connectivity, and promote recovery of strength after acute or chronic denervation due to injury, disease, or aging.

Indexed as

Hydroxyprostaglandin DehydrogenasesSynapsesAgedAnimalsDenervationHumansMiceMuscle, SkeletalNerve RegenerationProstaglandins15-hydroxyprostaglandin dehydrogenaseHydroxyprostaglandin DehydrogenasesProstaglandins

Identifiers

PMID37820010
PMCPMC10763629
OpenAlexW4387526346

What Socratic 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 Socratic graph.