Review articles

Publisher Website
Google Scholar
Abstract
Endothelial dysfunction is the final common pathway in the pathogenesis of preeclampsia. Future therapeutic modalities aimed at preventing or treating preeclampsia should either reduce the extent of (or even prevent) endothelial cell dysfunction (primary prevention) or should reduce the consequences of endothelial cell dysfunction (secondary and tertiary prevention). Relevant potential and promising directions for further research will be discussed. Part I of this review concerns the primary prevention of preeclampsia. The etiology of preeclampsia is still unknown. The 4 hypotheses that are the most popular currently are the placental ischemia hypothesis, the immune maladaptation/spiral artery-decidual ¿toxin' hypothesis, the VLDL (very low density lipoproteins)/TxPA (toxicity preventing activity) hypothesis, and the genetic hypothesis. For the near future only the disturbed VLDL/TxPA balance and the imbalance between free radicals and scavengers appear to be amenable for clinical research purposes.

This publication has 100 references indexed in Scilit: