ReviewAmerican journal of obstetrics and gynecology2016
New development of the yolk sac theory in diabetic embryopathy: molecular mechanism and link to structural birth defects.
Review in American journal of obstetrics and gynecology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 60 citations in OpenAlex.
- Periconceptional ultra-processed food consumption in women and men, fertility, and early embryonic development.Human reproduction (Oxford, England) · 2026Article
- CombinedActa biochimica et biophysica Sinica · 2025Article
- Maternal Circulatory NAD Precursor Levels and the Yolk Sac Determine NAD Deficiency-Driven Congenital Malformation Risk.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Impaired yolk sac NAD metabolism disrupts murine embryogenesis with relevance to human birth defects.eLife · 2025Article
- HucMSCs can alleviate abnormal vasculogenesis induced by high glucose through the MAPK signaling pathway.iScience · 2024Article
- Amniotic fluid-derived stem cells: potential factories of natural and mimetic strategies for congenital malformations.Stem cell research & therapy · 2024Article
- Redox Regulation of KAntioxidants & redox signaling · 2024Review
- Epidemiology of congenital malformations in Tunisian liveborns: a retrospective study.African health sciences · 2024Article
- Amniotic fluid-derived stem cells: potential factories of natural and mimetic strategies for congenital malformations.Research square · 2024Article
- MicroRNA-322 overexpression reduces neural tube defects in diabetic pregnancies.American journal of obstetrics and gynecology · 2024Article
- High amniotic fluid fractalkine and MIP-1β levels are associated with intrauterine growth restriction: a prospective cohort study.Turkish journal of medical sciences · 2024Article
- Phenotypically Discordant Anomalies in Conjoined Twins: Quirks of Nature Governed by Molecular Pathways?Diagnostics (Basel, Switzerland) · 2023Review
- Functional cargos of exosomes derived from Flk-1Communications biology · 2022Article
- Identification of novel candidate risk genes for myelomeningocele within the glucose homeostasis/oxidative stress and folate/one-carbon metabolism networks.Molecular genetics & genomic medicine · 2020Article
- Deficiency of the oxidative stress-responsive kinase p70S6K1 restores autophagy and ameliorates neural tube defects in diabetic embryopathy.American journal of obstetrics and gynecology · 2020Article
- Restoring BMP4 expression in vascular endothelial progenitors ameliorates maternal diabetes-induced apoptosis and neural tube defects.Cell death & disease · 2020Article
- Exposure-based assessment of chemical teratogenicity using morphogenetic aggregates of human embryonic stem cells.Reproductive toxicology (Elmsford, N.Y.) · 2020Article
- The increased activity of a transcription factor inhibits autophagy in diabetic embryopathy.American journal of obstetrics and gynecology · 2019Article
- High Glucose Inhibits Neural Stem Cell Differentiation Through Oxidative Stress and Endoplasmic Reticulum Stress.Stem cells and development · 2018Article
- Adverse effects of Hif1a mutation and maternal diabetes on the offspring heart.Cardiovascular diabetology · 2018Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Maternal diabetes mellitus is a significant risk factor for structural birth defects, including congenital heart defects and neural tube defects. With the rising prevalence of type 2 diabetes mellitus and obesity in women of childbearing age, diabetes mellitus-induced birth defects have become an increasingly significant public health problem. Maternal diabetes mellitus in vivo and high glucose in vitro induce yolk sac injuries by damaging the morphologic condition of cells and altering the dynamics of organelles. The yolk sac vascular system is the first system to develop during embryogenesis; therefore, it is the most sensitive to hyperglycemia. The consequences of yolk sac injuries include impairment of nutrient transportation because of vasculopathy. Although the functional relationship between yolk sac vasculopathy and structural birth defects has not yet been established, a recent study reveals that the quality of yolk sac vasculature is related inversely to embryonic malformation rates. Studies in animal models have uncovered key molecular intermediates of diabetic yolk sac vasculopathy, which include hypoxia-inducible factor-1α, apoptosis signal-regulating kinase 1, and its inhibitor thioredoxin-1, c-Jun-N-terminal kinases, nitric oxide, and nitric oxide synthase. Yolk sac vasculopathy is also associated with abnormalities in arachidonic acid and myo-inositol. Dietary supplementation with fatty acids that restore lipid levels in the yolk sac lead to a reduction in diabetes mellitus-induced malformations. Although the role of the human yolk in embryogenesis is less extensive than in rodents, nevertheless, human embryonic vasculogenesis is affected negatively by maternal diabetes mellitus. Mechanistic studies have identified potential therapeutic targets for future intervention against yolk sac vasculopathy, birth defects, and other complications associated with diabetic pregnancies.
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