Preeclampsia results from a complex interaction between immunological alterations, endothelial dysfunction, and insulin resistance. Inositol second messengers are known to be involved in metabolic signaling and are highly expressed during preeclampsia. In the past two decades, several studies were published on different aspects where these molecules are involved. It appears that maternal increase of IPG-P content in all tissues and fluids reflects an increased production of inositol mediators on the fetal side in preeclampsia. This comprehensive review of findings shows a possible role for these molecules as a link between metabolism, immunology, vascular alterations, predisposition to seizures, and cardiovascular disease later in life.
Keywords: Endothelial; Immunology; Insulin resistance; Metabolic Syndrome; Preeclampsia; Pregnancy.
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