Evidence map›Paper›PMID 29312475›Full record

ReviewOxidative medicine and cellular longevity2017

Molecular Mechanisms Responsible for Increased Vulnerability of the Ageing Oocyte to Oxidative Damage.

Bettina P Mihalas, Kate A Redgrove, Eileen A McLaughlin, Brett Nixon

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Oxidative medicine and cellular longevity, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing 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

52 citing papers in PubMed.

  1. Article
  2. Review
  3. Visible light, oxidative stress, and reproduction: The protective role of melatonin.International journal of gynaecology and obstetrics: the official organ of the International Federation of Gynaecology and Obstetrics · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Clocks and Dominoes: Timing Mechanisms of Embryogenesis.bioRxiv : the preprint server for biology · 2026
    Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Article
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  17. Article
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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.

Bettina P MihalasPriority Research Centre for Reproductive Science, School of Environmental and Life Sciences, University of Newcastle, Callaghan, NSW, Australia.ORCID 0000-0002-6006-8475
Kate A RedgrovePriority Research Centre for Reproductive Science, School of Environmental and Life Sciences, University of Newcastle, Callaghan, NSW, Australia.
Eileen A McLaughlinPriority Research Centre for Reproductive Science, School of Environmental and Life Sciences, University of Newcastle, Callaghan, NSW, Australia.
Brett NixonPriority Research Centre for Reproductive Science, School of Environmental and Life Sciences, University of Newcastle, Callaghan, NSW, Australia.ORCID 0000-0003-2745-8188

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In their midthirties, women experience a decline in fertility, coupled to a pronounced increase in the risk of aneuploidy, miscarriage, and birth defects. Although the aetiology of such pathologies are complex, a causative relationship between the age-related decline in oocyte quality and oxidative stress (OS) is now well established. What remains less certain are the molecular mechanisms governing the increased vulnerability of the aged oocyte to oxidative damage. In this review, we explore the reduced capacity of the ageing oocyte to mitigate macromolecular damage arising from oxidative insults and highlight the dramatic consequences for oocyte quality and female fertility. Indeed, while oocytes are typically endowed with a comprehensive suite of molecular mechanisms to moderate oxidative damage and thus ensure the fidelity of the germline, there is increasing recognition that the efficacy of such protective mechanisms undergoes an age-related decline. For instance, impaired reactive oxygen species metabolism, decreased DNA repair, reduced sensitivity of the spindle assembly checkpoint, and decreased capacity for protein repair and degradation collectively render the aged oocyte acutely vulnerable to OS and limits their capacity to recover from exposure to such insults. We also highlight the inadequacies of our current armoury of assisted reproductive technologies to combat age-related female infertility, emphasising the need for further research into mechanisms underpinning the functional deterioration of the ageing oocyte.

Indexed as

AgingOxidative StressDNA RepairFemaleGlycation End Products, AdvancedHumansMitochondriaM Phase Cell Cycle CheckpointsOocytesReactive Oxygen SpeciesGlycation End Products, AdvancedReactive Oxygen Species

Identifiers

PMID29312475
PMCPMC5664291

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.