Evidence map›Paper›PMID 25197655›Full record

ReviewBioMed research international2014

DNA damage and its cellular response in mother and fetus exposed to hyperglycemic environment.

Jusciele Brogin Moreli, Janine Hertzog Santos, Clarissa Ribeiro Rocha, Débora Cristina Damasceno, Glilciane Morceli, Marilza Vieira Rudge, Estela Bevilacqua, Iracema Mattos Paranhos Calderon

Open access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.9field-weighted citation impact, top 7% 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

14 citing papers in PubMed, 43 citations in OpenAlex.

  1. Trial
  2. AI-Driven Fetal Liver Echotexture Analysis: A New Frontier in Predicting Neonatal Insulin Imbalance.Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine · 2026
    Article
  3. Review
  4. Oxidative Stress in Pregnancy.Biomolecules · 2023
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

8 authors at 3 institutions in 2 countries.

Jusciele Brogin MoreliGraduate Program in Gynecology, Obstetrics and Mastology, Botucatu Medical School, São Paulo State University (UNESP), SP, Brazil.
Janine Hertzog SantosLaboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences (NIEHS), NC, USA.
Clarissa Ribeiro RochaDepartment of Microbiology, Institute of Biomedical Sciences, University of São Paulo (USP), SP, Brazil.
Débora Cristina DamascenoGraduate Program in Gynecology, Obstetrics and Mastology, Botucatu Medical School, São Paulo State University (UNESP), SP, Brazil.ORCID 0000-0002-7003-9643
Glilciane MorceliGraduate Program in Gynecology, Obstetrics and Mastology, Botucatu Medical School, São Paulo State University (UNESP), SP, Brazil.ORCID 0000-0001-8216-9931
Marilza Vieira RudgeGraduate Program in Gynecology, Obstetrics and Mastology, Botucatu Medical School, São Paulo State University (UNESP), SP, Brazil.
Estela BevilacquaDepartment of Cell and Developmental Biology, Institute of Biomedical Sciences, USP, University of São Paulo, São Paulo, Brazil.
Iracema Mattos Paranhos CalderonGraduate Program in Gynecology, Obstetrics and Mastology, Botucatu Medical School, São Paulo State University (UNESP), SP, Brazil ; Department of Obstetrics and Gynecology, Botucatu Medical School, São Paulo State University (UNESP), Distrito de Rubião Jr. s/n, 18618-000 Botucatu, SP, Brazil.
Universidade Estadual Paulista (Unesp) · BRUniversidade de São Paulo · BRNational Institute of Environmental Health Sciences · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The increased production of reactive oxygen species (ROS) plays a key role in pathogenesis of diabetic complications. ROS are generated by exogenous and endogenous factors such as during hyperglycemia. When ROS production exceeds the detoxification and scavenging capacity of the cell, oxidative stress ensues. Oxidative stress induces DNA damage and when DNA damage exceeds the cellular capacity to repair it, the accumulation of errors can overwhelm the cell resulting in cell death or fixation of genome mutations that can be transmitted to future cell generations. These mutations can lead to and/or play a role in cancer development. This review aims at (i) understanding the types and consequences of DNA damage during hyperglycemic pregnancy; (ii) identifying the biological role of DNA repair during pregnancy, and (iii) proposing clinical interventions to maintain genome integrity. While hyperglycemia can damage the maternal genetic material, the impact of hyperglycemia on fetal cells is still unclear. DNA repair mechanisms may be important to prevent the deleterious effects of hyperglycemia both in mother and in fetus DNA and, as such, prevent the development of diseases in adulthood. Hence, in clinical practice, maternal glycemic control may represent an important point of intervention to prevent the deleterious effects of maternal hyperglycemia to DNA.

Indexed as

DNA DamageDNA RepairFemaleFetusGenomic InstabilityHumansHyperglycemiaOxidative StressPregnancy

Identifiers

PMID25197655
PMCPMC4147359
OpenAlexW2109614330

What OpenQuestion 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 OpenQuestion graph.