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. 2017 May 5;8:247. doi: 10.3389/fphar.2017.00247

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Copyright © 2017 Katsi, Georgountzos, Kallistratos, Zerdes, Makris, Manolis, Nihoyannopoulos and Tousoulis.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The malfunction in the invasion of trophoblastic cells is thought to be fundamental in the cascade of preeclampsia. Also, the role of NO and HO/CO activity in the release of antiangiogenic factors sFlt-1 and sEng is crucial in the pathogenesis of the disease. By blocking these regulatory points, statins beneficially allow the synthesis of NO by eNOS, leading to vasodilation and decrease of the secretion of antiangiogenic factors. The latter effect results in the increase of VEGF and PIGF which are key components in placental and endothelial integrity. eNOS, endothelial nitric oxidase synthase; ET -1, endothelin 1; HO-1/CO, hemeoxygenase -1/ carbon monoxide; NO, nitric oxide; PIGF, placental growth factor; sEng, soluble endoglin; sFlt-1, soluble Fms- like tyrosine kinase; TGF – β, transforming growth factor β; VEGF, vascular endothelial growth factor.