Research ArticleDevelopment

Maternal Hyperglycemia Activates an ASK1–FoxO3a–Caspase 8 Pathway That Leads to Embryonic Neural Tube Defects

Science Signaling  27 Aug 2013:
Vol. 6, Issue 290, pp. ra74
DOI: 10.1126/scisignal.2004020

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Preventing Sugar-Induced Birth Defects

The central nervous system initially develops from an embryonic structure called the neural tube. Neural tube defects result when the neural tube does not close properly and can range in severity from spina bifida to anencephaly, which is fatal. Maternal hyperglycemia is associated with the development of neural tube defects. Yang et al. uncovered a signaling pathway initiated by apoptosis signal–regulating kinase 1 (ASK1) that was associated with an increased incidence of neural tube defects due to cell death in the embryos of diabetic mice. The incidence of neural tube defects was decreased by genetic ablation of ASK1 or the downstream components of this pathway, or by injecting pregnant mice with an inhibitor of ASK1. Thus, interfering with activation of the ASK1 signaling pathway could help to limit the development of neural tube defects in babies born to diabetic women.