A Review: Molecular Concepts and Common Pathways Involving Vitamin D in the Pathophysiology of Preeclampsia

Preeclampsia is one of the most serious conditions at the end of pregnancy, causing increased perinatal morbidity and mortality to the pregnant mother and her product of conception. It remains a high-risk disease in ethnic minorities worldwide. Conception involves fetal invasion and implantation, followed by an actively forming and shedding decidua, an important uterine activity facilitating placental development. Dysregulation in conception mediates functional changes that induce onset of preeclampsia. The pathophysiology of preeclampsia primarily results from impaired trophoblastic invasion and implantation with subsequent vasculopathy. These events trigger exaggerated ischemic, inflammatory and immunologic events in the placenta bed that disrupt implantation. As the underlying mechanism(s) of preeclampsia remain obscure, there is increasing evidence that Vitamin D deficiency during pregnancy potentiates hypertensive states that could lead to the development of preeclampsia. As a prohormone, Vitamin D regulates molecular events within central pathophysiological pathways of implantation and vascular development. We review shared pathways involving Vitamin D modulation of pathologic events in implantation associated with preeclampsia. Understanding the causal mechanisms between Vitamin D and preeclampsia during early stages of conception could allude to development of candidate markers for treatment or screening, and decipher “hot spots” for research and intervention of, at-risk pregnant mothers.