Evidence map›Paper›PMID 35986715›Full record

ReviewMolecular reproduction and development2023

The role of mtDNA in oocyte quality and embryo development.

Justin C St John, Takashi Okada, Eryk Andreas, Alexander Penn

Abstract readReview
In one paragraph

Review in Molecular reproduction and development, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
–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

20 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. EndoCompass Project: Endocrinology across the Lifespan.Hormone research in paediatrics · 2025
    Review
  12. Review
  13. Article
  14. AMPK Suppression Due to Obesity Drives Oocyte mtDNA Heteroplasmy via ATF5-POLG Axis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  15. Article
  16. The role of mtDNA in oocyte quality and embryo development.Molecular reproduction and development · 2023
    Review
  17. Article
  18. Review
  19. Mitochondrial DNA Deficiency and Supplementation inInternational journal of molecular sciences · 2023
    Article
  20. 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

4 authors.

Justin C St JohnThe Mitochondrial Genetics Group, The School of Biomedicine and The Robinson Research Institute, The University of Adelaide, Adelaide, South Australia, Australia.
Takashi OkadaThe Mitochondrial Genetics Group, The School of Biomedicine and The Robinson Research Institute, The University of Adelaide, Adelaide, South Australia, Australia.
Eryk AndreasThe Mitochondrial Genetics Group, The School of Biomedicine and The Robinson Research Institute, The University of Adelaide, Adelaide, South Australia, Australia.
Alexander PennThe Mitochondrial Genetics Group, The School of Biomedicine and The Robinson Research Institute, The University of Adelaide, Adelaide, South Australia, Australia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The mitochondrial genome resides in the mitochondria present in nearly all cell types. The porcine (Sus scrofa) mitochondrial genome is circa 16.7 kb in size and exists in the multimeric format in cells. Individual cell types have different numbers of mitochondrial DNA (mtDNA) copy number based on their requirements for ATP produced by oxidative phosphorylation. The oocyte has the largest number of mtDNA of any cell type. During oogenesis, the oocyte sets mtDNA copy number in order that sufficient copies are available to support subsequent developmental events. It also initiates a program of epigenetic patterning that regulates, for example, DNA methylation levels of the nuclear genome. Once fertilized, the nuclear and mitochondrial genomes establish synchrony to ensure that the embryo and fetus can complete each developmental milestone. However, altering the oocyte's mtDNA copy number by mitochondrial supplementation can affect the programming and gene expression profiles of the developing embryo and, in oocytes deficient of mtDNA, it appears to have a positive impact on the embryo development rates and gene expression profiles. Furthermore, mtDNA haplotypes, which define common maternal origins, appear to affect developmental outcomes and certain reproductive traits. Nevertheless, the manipulation of the mitochondrial content of an oocyte might have a developmental advantage.

Indexed as

DNA, MitochondrialOocytesEmbryonic DevelopmentMitochondriaOogenesisDNA, Mitochondrialgenomic balancemitochondrial DNAmitochondrial supplementationnuclear transferoogenesis

Identifiers

PMID35986715
PMCPMC10952685

What OpenQuestion holds

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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.