Evidence map›Paper›PMID 20706996›Full record

ReviewBirth defects research. Part A, Clinical and molecular teratology2010

Understanding diabetic teratogenesis: where are we now and where are we going?

Sheller Zabihi, Mary R Loeken

Open access · greenAbstract readReview
In one paragraph

Review in Birth defects research. Part A, Clinical and molecular teratology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
6.0field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 100 citations in OpenAlex.

  1. Article
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  3. Article
  4. Review
  5. Article
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  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Skeletal malformations and growth disturbances in fetuses of mild diabetic ratsBiomedica : revista del Instituto Nacional de Salud · 2021
    Article
  13. Review
  14. Dysglycemia in Pregnancy and Maternal/Fetal Outcomes.Journal of women's health (2002) · 2021
    Article
  15. Review
  16. Article
  17. Aberrant DNA methylation as a diagnostic biomarker of diabetic embryopathy.Genetics in medicine : official journal of the American College of Medical Genetics · 2019
    Article
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Sheller ZabihiSection on Developmental and Stem Cell Biology, Joslin Diabetes Center, One Joslin Place, Boston, MA 02215, USA.
Mary R Loeken
Joslin Diabetes Center · US

Funding

SEARCH FOR THE MOLECULAR CAUSES OF DIABETIC EMBRYOPATHYR01DK052865 · NIDDK · JOSLIN DIABETES CENTER · PI LOEKEN, MARY R · 1998 to 2013
$4.4M
MOLECULAR REGULATION: EMBYROGENESIS BY METABOLIC STRESSR01DK058300 · NIDDK · JOSLIN DIABETES CENTER · PI LOEKEN, MARY R · 2000 to 2014
$4.3M
NIDDK NIH HHS R01 DK052865NIDDK NIH HHS R01 DK058300NIDDK NIH HHS R01 DK52865NIDDK NIH HHS R01 DK58300
6 · The paper itself

Abstract

Maternal pregestational diabetes (type 1 or type 2) poses an increased risk for a broad spectrum of birth defects. To our knowledge, this problem first came to the attention of the Teratology Society at the 14th Annual Meeting in Vancouver, B.C. in 1974, with a presentation by Lewis Holmes, "Etiologic heterogeneity of neural tube defects". Although advances in the control of diabetes in the decades since the discovery of insulin in the 1920's have reduced the risk for birth defects during diabetic pregnancy, the increasing incidence of diabetes among women of childbearing years indicates that this cause of birth defects is a growing public health concern. Major advances in understanding how a disease of maternal fuel metabolism can interfere with embryogenesis of multiple organ systems have been made in recent years. In this review, we trace the history of the study of diabetic teratogenesis and discuss a model in which tissue-specific developmental control genes are regulated at specific times in embryonic development by glucose metabolism. The major function of such genes is to suppress apoptosis, perhaps to preserve proliferative capability, and inhibit premature senescence.

Indexed as

AnimalsApoptosisCongenital AbnormalitiesDiabetes Mellitus, ExperimentalDiabetes Mellitus, Type 1Diabetes Mellitus, Type 2Embryonic DevelopmentFemaleFetal DiseasesGene Expression Regulation, DevelopmentalGenes, p53HumansHyperglycemiaMiceMice, KnockoutNeural Tube DefectsPaired Box Transcription FactorsPAX3 protein, humanPAX3 Transcription FactorTeratogens

Identifiers

PMID20706996
PMCPMC5070114
OpenAlexW1512266982

What OpenQuestion holds

Textmetadata
LicenceTDM
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.