Evidence map›Paper›PMID 38769369›Full record

ArticleCommunications biology2024

GDE5/Gpcpd1 activity determines phosphatidylcholine composition in skeletal muscle and regulates contractile force in mice.

Rahmawati Aisyah, Noriyasu Ohshima, Daiki Watanabe, Yoshiko Nakagawa, Tetsushi Sakuma, Felix Nitschke, Minako Nakamura, Koji Sato, Kaori Nakahata, Chihiro Yokoyama and 12 more

Abstract read
In one paragraph

Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed.

  1. Trial
  2. Article
  3. Review
  4. Ionic-Bionic Interfaces: Advancing Iontronic Strategies for Bioelectronic Sensing and Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. 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

22 authors.

Rahmawati Aisyah *Graduate School of Integrated Sciences for Life, Hiroshima University, Hiroshima, Japan.
Noriyasu Ohshima *Graduate School of Medicine, Gunma University, Gunma, Japan.ORCID 0000-0002-6752-2490
Daiki Watanabe *Graduate School of Humanities and Social Sciences, Hiroshima University, Hiroshima, Japan.
Yoshiko NakagawaCenter for Animal Resources and Development (CARD), Kumamoto University, Kumamoto, Japan.
Tetsushi SakumaGraduate School of Integrated Sciences for Life, Hiroshima University, Hiroshima, Japan.ORCID 0000-0003-0396-1563
Felix NitschkeDepartment of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, USA.ORCID 0000-0002-1118-2693
Minako NakamuraGraduate School of Integrated Sciences for Life, Hiroshima University, Hiroshima, Japan.
Koji SatoGraduate School of Integrated Sciences for Life, Hiroshima University, Hiroshima, Japan.
Kaori NakahataGraduate School of Integrated Sciences for Life, Hiroshima University, Hiroshima, Japan.
Chihiro YokoyamaGraduate School of Integrated Sciences for Life, Hiroshima University, Hiroshima, Japan.
Charlotte R MarchioniDepartment of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Thanutchaporn KumrungseeGraduate School of Integrated Sciences for Life, Hiroshima University, Hiroshima, Japan.ORCID 0000-0002-6196-5186
Takahiko ShimizuAging Stress Response Research Project Team, National Center for Geriatrics and Gerontology, Aichi, Japan.
Yusuke SotomaruNatural Science Center for Basic Research and Development, Hiroshima University, Hiroshima, Japan.ORCID 0000-0002-2856-1518
Toru TakeoCenter for Animal Resources and Development (CARD), Kumamoto University, Kumamoto, Japan.ORCID 0000-0002-8103-651X
Naomi NakagataCenter for Animal Resources and Development (CARD), Kumamoto University, Kumamoto, Japan.ORCID 0000-0002-5737-9993
Takashi IzumiGraduate School of Medicine, Gunma University, Gunma, Japan.ORCID 0000-0002-4268-1874
Shinji MiuraGraduate School of Nutritional and Environmental Sciences, University of Shizuoka, Shizuoka, Japan.ORCID 0000-0001-8806-9763
Berge A MinassianDepartment of Pediatrics, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Takashi YamamotoGraduate School of Integrated Sciences for Life, Hiroshima University, Hiroshima, Japan.
Masanobu WadaGraduate School of Humanities and Social Sciences, Hiroshima University, Hiroshima, Japan.
Noriyuki YanakaGraduate School of Integrated Sciences for Life, Hiroshima University, Hiroshima, Japan. yanaka@hiroshima-u.ac.jp.ORCID 0000-0002-9564-0822

Funding

Uncovering cellular mechanisms to keep glycogen water-solubleR01NS128437 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI Felix Nitschke · 2022 to 2026
$2.0M
MEXT | Japan Society for the Promotion of Science (JSPS) 21H02139NINDS NIH HHS R01 NS128437
6 · The paper itself

Abstract

Glycerophosphocholine (GPC) is an important precursor for intracellular choline supply in phosphatidylcholine (PC) metabolism. GDE5/Gpcpd1 hydrolyzes GPC into choline and glycerol 3-phosphate; this study aimed to elucidate its physiological function in vivo. Heterozygous whole-body GDE5-deficient mice reveal a significant GPC accumulation across tissues, while homozygous whole-body knockout results in embryonic lethality. Skeletal muscle-specific GDE5 deletion (Gde5 skKO) exhibits reduced passive force and improved fatigue resistance in electrically stimulated gastrocnemius muscles in vivo. GDE5 deficiency also results in higher glycolytic metabolites and glycogen levels, and glycerophospholipids alteration, including reduced levels of phospholipids that bind polyunsaturated fatty acids (PUFAs), such as DHA. Interestingly, this PC fatty acid compositional change is similar to that observed in skeletal muscles of denervated and Duchenne muscular dystrophy mouse models. These are accompanied by decrease of GDE5 expression, suggesting a regulatory role of GDE5 activity for glycerophospholipid profiles. Furthermore, a DHA-rich diet enhances contractile force and lowers fatigue resistance, suggesting a functional relationship between PC fatty acid composition and muscle function. Finally, skinned fiber experiments show that GDE5 loss increases the probability of the ryanodine receptor opening and lowers the maximum Ca

Indexed as

Mice, KnockoutMuscle ContractionMuscle, SkeletalPhosphatidylcholinesAnimalsMaleMiceMice, Inbred C57BLPhosphoric Diester Hydrolasesglycerophosphodiester phosphodiesterasePhosphatidylcholinesPhosphoric Diester Hydrolases

Identifiers

PMID38769369
PMCPMC11106330

What OpenQuestion holds

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Registered trials

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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.