ArticleBiochemical and biophysical research communications2016
Identification of novel cell survival regulation in diabetic embryopathy via phospholipidomic profiling.
Article in Biochemical and biophysical research communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Maternal diabetes-associated neural tube defects: evidence for β-hydroxybutyrate-related HDAC1/3-H3K27ac-MEST-LRP6 dysregulation.Frontiers in physiology · 2026Article
- miR‑29 promotes the proliferation of cultured rat neural stem/progenitor cells via the PTEN/AKT signaling pathway.Molecular medicine reports · 2019Article
- Impact of protein O-GlcNAcylation on neural tube malformation in diabetic embryopathy.Scientific reports · 2017Article
- Formation of neurodegenerative aggresome and death-inducing signaling complex in maternal diabetes-induced neural tube defects.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Diabetes mellitus in early pregnancy causes birth defects by disturbing metabolic homeostasis and increasing programmed cell death in the embryo. Over-activation of phospholipase Cβ3 and γ1 suggests disturbed phospholipid metabolism, which is an important in regulation of cell signaling and activity. Metabolomic examinations reveal significant changes in the profile of phospholipid metabolism. Among the metabolites, levels of phosphatidylinositol bisphosphate (PIP2) are increased. PIP2 effector PTEN (phosphatase and tensin homolog deleted on chromosome 10) is activated. Activation of protein kinase Bα (PKBα, or AKT1) and mTOR (mechanistic target of rapamycin) is decreased. Inhibition of PLCs and PTEN suppresses over-generation of reactive oxygen species and inhibition of PLCs prevents fragmentation of mitochondria in neural stem cells cultured in high glucose. These observations suggest that maternal hyperglycemia disrupts phospholipid metabolism, leading to perturbation of mitochondrial dynamics and redox homeostasis and suppression of the PKB-mTOR cell survival signaling in the embryos.
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Registered trials
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