Abstract
Embryonic malformation in diabetic pregnancy, including neural tube defects, are associated with oxidative stress and activation of stress-response pathways including the c-Jun N-terminal kinase (JNK), Akt, and Toll Like Receptor 4 (TLR4) pathways. Protein kinase C (PKC) family members, including PKCδ, have been implicated in diabetic embryopathy.
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