Evidence map›Paper›PMID 33264618›Full record

ArticleCell reports2020

Maternal Inactivity Programs Skeletal Muscle Dysfunction in Offspring Mice by Attenuating Apelin Signaling and Mitochondrial Biogenesis.

Jun Seok Son, Song Ah Chae, Hongyang Wang, Yanting Chen, Alejandro Bravo Iniguez, Jeanene M de Avila, Zhihua Jiang, Mei-Jun Zhu, Min Du

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

35 citing papers in PubMed, 50 citations in OpenAlex.

  1. Trial
  2. Myokines and mitochondrial function in cardiometabolic diseases.Journal of physiology and biochemistry · 2026
    Review
  3. Article
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Exercise attenuates polycystic ovary syndrome development via improved mitochondrial proteostasis.American journal of physiology. Endocrinology and metabolism · 2026
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. Skeletal Muscle as Endocrine Organ.Advances in experimental medicine and biology · 2025
    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 2 institutions in 2 countries.

Jun Seok SonNutrigenomics and Growth Biology Laboratory, Department of Animal Sciences, Washington State University, Pullman, WA 99164, USA; School of Molecular Biosciences, Washington State University, Pullman, WA 99164, USA.
Song Ah ChaeNutrigenomics and Growth Biology Laboratory, Department of Animal Sciences, Washington State University, Pullman, WA 99164, USA.
Hongyang WangInstitute of Animal Husbandry and Veterinary Science, Shanghai Academy of Agricultural Sciences, Shanghai, China.
Yanting ChenNutrigenomics and Growth Biology Laboratory, Department of Animal Sciences, Washington State University, Pullman, WA 99164, USA.
Alejandro Bravo IniguezSchool of Food Science, Washington State University, Pullman, WA 99164, USA.
Jeanene M de AvilaNutrigenomics and Growth Biology Laboratory, Department of Animal Sciences, Washington State University, Pullman, WA 99164, USA.
Zhihua JiangNutrigenomics and Growth Biology Laboratory, Department of Animal Sciences, Washington State University, Pullman, WA 99164, USA.
Mei-Jun ZhuSchool of Food Science, Washington State University, Pullman, WA 99164, USA.
Min DuNutrigenomics and Growth Biology Laboratory, Department of Animal Sciences, Washington State University, Pullman, WA 99164, USA; School of Molecular Biosciences, Washington State University, Pullman, WA 99164, USA. Electronic address: min.du@wsu.edu.
Washington State University · USShanghai Academy of Agricultural Sciences · CN

Funding

Maternal obesity, AMPK and fetal brown adipogenesisR01HD067449 · NICHD · WASHINGTON STATE UNIVERSITY · PI MIN DU · 2010 to 2026
$4.6M
NICHD NIH HHS R01 HD067449
6 · The paper itself

Abstract

Although maternal exercise (ME) becomes increasingly uncommon, the effects of ME on offspring muscle metabolic health remain largely undefined. Maternal mice are subject to daily exercise during pregnancy, which enhances mitochondrial biogenesis during fetal muscle development; this is correlated with higher mitochondrial content and oxidative muscle fibers in offspring muscle and improved endurance capacity. Apelin, an exerkine, is elevated due to ME, and maternal apelin administration mirrors the effect of ME on mitochondrial biogenesis in fetal muscle. Importantly, both ME and apelin induce DNA demethylation of the peroxisome proliferator-activated receptor γ coactivator-1α (Ppargc1a) promoter and enhance its expression and mitochondrial biogenesis in fetal muscle. Such changes in DNA methylation were maintained in offspring, with ME offspring muscle expressing higher levels of PGC-1α1/4 isoforms, explaining improved muscle function. In summary, ME enhances DNA demethylation of the Ppargc1a promoter in fetal muscle, which has positive programming effects on the exercise endurance capacity and protects offspring muscle against metabolic dysfunction.

Indexed as

Organelle BiogenesisAnimalsApelinDisease Models, AnimalFemaleMiceMitochondriaMuscle, SkeletalPregnancySignal TransductionApelinapelinDNA methylationendurance capacityfetusmaternal exercisemitochondrial biogenesismuscleoxidative fibersPGC-1αpregnancy

Identifiers

PMID33264618
PMCPMC8137280
OpenAlexW3108250923

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.