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Updated: Dec 31, 2025
Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles
Published on: January 26, 2024
Oxidative stress in pregnancy complicated by preeclampsia
Sindy San Juan-Reyes1, Leobardo Manuel Gómez-Oliván1, Hariz Islas-Flores1
1Laboratorio de Toxicología Ambiental, Facultad de Química, Universidad Autónoma del Estado de México, Paseo Colón intersección Paseo Tollocan s/n, Col. Residencial Colón, 50120, Toluca, Estado de México, Mexico.
Insights
Preeclampsia, a pregnancy disorder, involves oxidative stress (OS) damaging the placenta and leading to maternal endothelial dysfunction. This review explores OS as a key factor in preeclampsia development and its associated risks.
Area of Science:
- Obstetrics and Gynecology
- Perinatal Medicine
- Pathophysiology
Background:
- Preeclampsia is a serious pregnancy complication causing significant perinatal morbidity and mortality.
- Recent research highlights key pathophysiological mechanisms including immune response alterations, endothelial dysfunction, oxidative stress, and genetic factors.
- Oxidative stress (OS) is implicated in placental remodeling issues and vascular endothelial dysfunction, leading to ischemia/reperfusion injury.
Purpose of the Study:
- To review the primary risk factors associated with preeclampsia.
- To elucidate the role of oxidative stress (OS) as a central pathophysiological mechanism in preeclampsia development.
Main Methods:
- Literature review of studies published in the last decade.
- Analysis of key pathophysiological mechanisms contributing to preeclampsia.
- Focus on the role of oxidative stress and reactive oxygen species (ROS) generation.
Main Results:
- Oxidative stress significantly impacts placental development and function.
- Increased xanthine oxidase activity leads to elevated reactive oxygen species (ROS) production.
- ROS contribute to cellular damage, inflammation, and maternal systemic endothelial dysfunction.
Conclusions:
- Oxidative stress is a critical factor in the pathophysiology of preeclampsia.
- Understanding OS mechanisms is vital for identifying preeclampsia risk factors and potential interventions.
Abstract:
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 dysfunction, 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, mitochondria, 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 inflammatory 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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