Potential Mechanisms Involved in Diabetic Teratogenesis During Embryonic Neural Tube Closure
Potential Mechanisms Involved in Diabetic Teratogenesis During Embryonic Neural Tube Closure
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Corresponding Author
Janice BlockMercaz HaBriut, Center for Integrative Medicine, Nahal Achziv 8/2, Ramat Beit, Shemesh, Israel
A B S T R A C T
Diabetes mellitus during pregnancy is a risk factor for improper closure of the neural tube during embryonic development. It is likely that this occurs via several parallel pathways. Previously proposed pathways for diabetic teratogenesis during neural tube closure include augmented production of nitric acid; reduction of Pax3; and increased production of long-chain acyl-CoA synthetase 1 (ACSL1). In the current discussion, an additional hypothesis is offered: that hyperglycemia might exert its teratogenic effects on the developing embryo via overexpression of collagen IV, leading to collagen imbalance and errors of remodelling.
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Research ArticlePublication history
Received: Wed 04, Sep 2019Accepted: Mon 23, Sep 2019
Published: Mon 30, Sep 2019
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© 2023 Janice Block. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Hosting by Science Repository.DOI: 10.31487/j.JDMC.2019.01.06