Evidence map›Paper›PMID 30231482›Full record

ArticleInternational journal of molecular sciences2018

ATP-Induced Increase in Intracellular Calcium Levels and Subsequent Activation of mTOR as Regulators of Skeletal Muscle Hypertrophy.

Naoki Ito, Urs T Ruegg, Shin'ichi Takeda

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed, 1 pooled it
5.2field-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

49 citing papers in PubMed, 1 synthesis or guideline pooled it, 80 citations in OpenAlex.

  1. Pooled it
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  14. Purinergic system in cancer stem cells.Purinergic signalling · 2025
    Review
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  18. TheMetabolites · 2024
    Article
  19. Review
  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

3 authors at 2 institutions in 2 countries.

Naoki ItoDepartment of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira 187-8502, Japan. naoki.ito.198571@gmail.com.ORCID 0000-0002-1884-8494
Urs T RueggPharmacology, Geneva-Lausanne School of Pharmaceutical Sciences, University of Geneva, CH 1211 Geneva, Switzerland. urs.ruegg@unige.ch.
Shin'ichi TakedaDepartment of Molecular Therapy, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira 187-8502, Japan. takeda@ncnp.go.jp.
National Center of Neurology and Psychiatry · JPUniversity of Geneva · CH

Funding

Intramural Research Grant for Neurological and Psychiatric Disorders of NCNP 28-6Japan Society for the Promotion of Science 11J04790Japan Society for the Promotion of Science 25282202
6 · The paper itself

Abstract

Intracellular signaling pathways, including the mammalian target of rapamycin (mTOR) and the mitogen-activated protein kinase (MAPK) pathway, are activated by exercise, and promote skeletal muscle hypertrophy. However, the mechanisms by which these pathways are activated by physiological stimulation are not fully understood. Here we show that extracellular ATP activates these pathways by increasing intracellular Ca

Indexed as

Adenosine TriphosphateAnimalsCalciumCell LineHypertrophyMaleMice, Inbred C57BLMuscle, SkeletalMuscular AtrophyTOR Serine-Threonine KinasesAdenosine TriphosphateCalciummTOR protein, mouseTOR Serine-Threonine KinasesATPCa2+IP3 receptormammalian target of rapamycin (mTOR)mitogen-activated protein kinase (MAPK)muscle atrophymuscle hypertrophyP2Y receptorskeletal muscle

Identifiers

PMID30231482
PMCPMC6163678
OpenAlexW2890577472

What Socratic 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 Socratic graph.