PATHOPHYSIOLOGY OF PREECLAMPSIA: MOLECULAR MECHANISMS AND MATERNAL-FETAL IMPLICATIONS

Abstract

Preeclampsia is a hypertensive syndrome specific to pregnancy, usually diagnosed after the 20th week, characterized by arterial hypertension associated with proteinuria or signs of maternal organ dysfunction. It is a complex and multifactorial condition with a significant impact on maternal and fetal morbidity and mortality worldwide. The understanding of its pathophysiology has evolved, highlighting the central role of alterations in placentation, endothelial dysfunction, and molecular imbalances that compromise vascular homeostasis. The objective of this summary is to describe the main molecular mechanisms involved in the pathophysiology of preeclampsia and discuss their implications for maternal-fetal health. The methodology is based on a narrative review of the scientific literature, considering both classic and recent studies on the pathophysiological, molecular, and clinical aspects of preeclampsia, focusing on articles published in recognized biomedical databases.The results show that the pathophysiology of preeclampsia occurs in two main phases. The first involves inadequate placentation, characterized by insufficient invasion of the extravillous trophoblast into the uterine spiral arteries, resulting in high-resistance vessels and low blood flow. This leads to placental hypoxia and oxidative stress. In the second phase, antiangiogenic factors are released into the maternal circulation, such as sFlt-1 (soluble fms-like tyrosine kinase-1) and soluble endoglin, which antagonize pro-angiogenic factors such as VEGF and PlGF. This imbalance promotes systemic endothelial dysfunction, increased vascular permeability, vasoconstriction, and inflammatory activation. Additionally, pro-inflammatory cytokines, reactive oxygen species, and alterations in maternal immune regulation participate in the disease process.The discussion demonstrates that these molecular mechanisms explain the clinical manifestations of the disease, including hypertension, proteinuria, edema, and severe complications such as eclampsia and HELLP syndrome. From the fetal perspective, reduced uteroplacental blood flow can lead to intrauterine growth restriction, prematurity, and fetal hypoxia. The identification of angiogenic biomarkers has contributed to early diagnosis and risk stratification, although limitations in broad clinical application remain.In conclusion, preeclampsia is a systemic condition originating in the placenta, mediated by complex molecular interactions that result in maternal endothelial dysfunction and fetal compromise. Advances in understanding these mechanisms are essential for the development of more effective preventive, diagnostic, and therapeutic strategies.