Resumen:
Preeclampsia is a multisystemic disorder of pregnancy that causes perinatal morbidity and mortality. Studies published in the last decade have contributed to a better understanding of physiopathogenesis through key mechanisms involved, such as altered immune response, endothelial dysfunction, oxidative stress and systemic inflammatory response, as well as genetic susceptibility. Oxidative stress (OS) plays an important role in the development of preeclampsia, since it alters placental remodeling and placental vascular endothelial dysfunc- tion, resulting in an ischemia/reperfusion injury with an increase in xanthine oxidase activity that produces high levels of reactive oxygen species (ROS). ROS can be generated through many pathways within cells, mi- tochondria, endoplasmic reticulum (ER) and enzymes such as NADPH oxidase are the most important sources, causing widespread and indiscriminate damage to cells and tissues, which leads to an intravascular in- flammatory response and maternal systemic endothelial dysfunction characteristic of this prenatal syndrome. Therefore, the following review aims to identify the main risk factors and the role of OS as a pathophysiological mechanism in the development of preeclampsia.
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