The role of molecular factors in gestational hypertension and the pathogenesis of preeclampsia

Preeclampsia (PE) is classified as a systemic condition that generally develops with high blood pressure and protein excretion in pregnant women after 20 weeks. This condition is characterised by inadequate placental blood flow and damages several organs. The illness is a complicated ailment that starts with an aberrant trophoblast invasion of the uterine decidua, endothelial dysfunction, and platelet aggregation, finally leading to a faulty placenta. Defective placenta causes difficulties such as hypoxia, oxidative stress, stimulation of the mother's immune system, and some other situations. Although the specific origin of this illness has not yet been discovered, various cellular signalling pathways may be implicated in its development. One of the molecules that may be implicated in preeclampsia is the sFlt-1 molecule. This protein has an inhibitory influence on vascularization of the placenta by lowering signalling VEGF, which leads to apoptosis of foetal vascular and disrupted placenta and exchange of nutrients, which finally leads to foetal growth limitation and preeclampsia. The renin-angiotensin-aldosterone pathway, inflammatory cytokines, and the Nrf2/HO-1 pathway are also implicated in the pathophysiology of this condition. The biogenesis route of microRNAs involved in controlling gene expression might be regarded as extra variables implicated in preeclampsia. The goal of this work was to elucidate the molecular components involved in the pathophysiology of preeclampsia.