Pregnancy Induced Hypertension and Preeclampsia- Pathophysiological Mystery and Molecular Phenomenon. 1800-OG-EN-PIHaP

One of three leading causes of maternal morbidity and mortality worldwide is PIH/preeclampsia, which afflicts 2-8% and is the most common cause of gestational hypertension.This subject is focused on pathophysiology and molecular mechanisms in normal and pathological spiral arteries remodeling and development of preeclampsia, with evaluation if certain molecules are promising therapeutic target.Molecular agents are key mediator of-lamentation Since insemination, it stimulates production of proinflammatory cytokines by uterine epithelium, which leads to activation of macrophages, uterine natural killer cells and other leukocytes. The trophblast/uNK/macrophage crosstalk is crucial for implantation and spiral arteries remodeling and NF-κB and NLRP3 regulates that process through modification of cytokine expression, as well as cell phenotype and function. In course of preeclampsia the remodeling processes is disturbed by excessive inflammation and increased NF-κB activation. The pathological remodeling leads to uteroplacental disfunction, release of pro inflammatory cytokinesinto the maternal circulation, endothelial stress and development of preeclampsia.The analysis of genetic and environmental inductors of NF-κB and NLRP3 helps to distinguish preeclampsia risk groups.Furthermore, a selective inhibition of NF-κB and NLRP3 activating pathways alleviates symptoms of preeclampsia in rat models, therefore, if properly balanced , this could be an efficient therapeutic option.