ReviewBirth defects research. Part A, Clinical and molecular teratology2011
Diabetic embryopathy: a role for the epigenome?
Review in Birth defects research. Part A, Clinical and molecular teratology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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.
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.
Who cites it
14 citing papers in PubMed, 39 citations in OpenAlex.
- Maternal sociodemographic characteristics, early pregnancy behaviours, and livebirth outcomes as congenital heart defects risk factors - Northern Ireland 2010-2014.BMC pregnancy and childbirth · 2021Article
- Intrauterine Programming of Diabetes Induced Cardiac Embryopathy.Diabetes & obesity international journal · 2019Article
- Embryonic defence mechanisms against glucose-dependent oxidative stress require enhanced expression of Alx3 to prevent malformations during diabetic pregnancy.Scientific reports · 2017Article
- Maternal diabetes modulates dental epithelial stem cells proliferation and self-renewal in offspring through apurinic/apyrimidinicendonuclease 1-mediated DNA methylation.Scientific reports · 2017Article
- Folates in Plants: Research Advances and Progress in Crop Biofortification.Frontiers in chemistry · 2017Review
- Prepregnancy Diabetes and Offspring Risk of Congenital Heart Disease: A Nationwide Cohort Study.Circulation · 2016Article
- The status of diabetic embryopathy.Upsala journal of medical sciences · 2016Review
- High glucose-induced oxidative stress represses sirtuin deacetylase expression and increases histone acetylation leading to neural tube defects.Journal of neurochemistry · 2016Article
- Gene expression in teratogenic exposures: a new approach to understanding individual risk.Reproductive toxicology (Elmsford, N.Y.) · 2014Article
- Variation in ultraviolet radiation and diabetes: evidence of an epigenetic effect that modulates diabetics' lifespan.Clinical epigenetics · 2013Article
- Diabetic embryopathy: a developmental perspective from fertilization to adulthood.Molecular syndromology · 2013Article
- Responses of the embryonic epigenome to maternal diabetes.Birth defects research. Part A, Clinical and molecular teratology · 2012Article
- Genetic and epigenomic footprints of folate.Progress in molecular biology and translational science · 2012Review
- Fetoplacental vascular endothelial dysfunction as an early phenomenon in the programming of human adult diseases in subjects born from gestational diabetes mellitus or obesity in pregnancy.Experimental diabetes research · 2011Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Embryonic development under adverse conditions, such as maternal diabetes or obesity during pregnancy, constitutes a major risk factor for birth defects, as well as for long-term health consequences and disease susceptibility in the offspring. While contributions from epigenetic changes have been invoked previously to explain the long-term changes in terms of developmental programming, we here review how maternal metabolism may directly affect the embryonic epigenome in relationship to teratogenic processes. We consider four epigenetic modalities--DNA methylation, non-coding RNA, transcription factors, and histone modifications--and their contribution to epigenetic memory, and discuss how epigenomic changes may mediate the altered control of embryonic gene expression brought about by maternal diabetes. In combination, the epigenomic modalities serve to define transcription-permissive domains of the genome, resulting in distinct epigenomic landscapes in different developmental cell types. We evaluate experimental approaches to characterize the epigenome in adverse pregnancy conditions, highlighting the role of next-generation sequencing on the technological side, while emphasizing the necessity to study defined cell populations in terms of biologic impact. Finally, we outline the challenges in moving from findings that correlate epigenomics to developmental phenotypes to scenarios that establish teratogenic causality.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.