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Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles
Published on: January 26, 2024
A Narrative Review on the Pathophysiology of Preeclampsia
Johnatan Torres-Torres1,2, Salvador Espino-Y-Sosa1, Raigam Martinez-Portilla1
1Clinical Research Branch, Instituto Nacional de Perinatología Isidro Espinosa de los Reyes, Mexico City 11000, Mexico.
Insights
Preeclampsia, a pregnancy disorder, stems from poor placentation, leading to maternal and fetal health risks. Understanding its complex causes like oxidative stress and inflammation is key to developing new treatments.
Area of Science:
- Reproductive Medicine and Obstetrics
- Pathophysiology of Pregnancy Complications
- Molecular and Cellular Biology
Background:
- Preeclampsia (PE) is a serious pregnancy disorder marked by hypertension and proteinuria.
- Its complex pathophysiology, involving multiple factors, is not fully understood.
- Current understanding highlights risks to both maternal and fetal well-being.
Purpose of the Study:
- To review and clarify the intricate mechanisms underlying preeclampsia.
- To focus on abnormal placentation, maternal systemic responses, oxidative stress, inflammation, and genetic/epigenetic factors.
- To synthesize recent findings on molecular and cellular pathways involved in PE.
Main Methods:
- Narrative review synthesizing data from recent studies, clinical trials, and meta-analyses.
- Integration of findings on oxidative stress biomarkers, angiogenic factors, immune interactions, and mitochondrial dysfunction.
- Analysis of genetic and epigenetic factors, including gene polymorphisms and microRNA expression.
Main Results:
- PE originates from poor placentation, leading to placental hypoxia and release of anti-angiogenic factors (sFlt-1, sEng).
- This causes endothelial dysfunction, systemic inflammation, oxidative stress, and immune dysregulation.
- Genetic factors like FLT1 polymorphisms and altered miRNA expression are critical.
Conclusions:
- Preeclampsia is a complex, multifactorial disorder involving abnormal placentation, endothelial dysfunction, inflammation, and oxidative stress.
- Emerging therapies targeting these pathways show promise.
- Further research is crucial for developing effective prevention and treatment strategies.
Abstract:
Preeclampsia (PE) is a multifactorial pregnancy disorder characterized by hypertension and proteinuria, posing significant risks to both maternal and fetal health. Despite extensive research, its complex pathophysiology remains incompletely understood. This narrative review aims to elucidate the intricate mechanisms contributing to PE, focusing on abnormal placentation, maternal systemic response, oxidative stress, inflammation, and genetic and epigenetic factors. This review synthesizes findings from recent studies, clinical trials, and meta-analyses, highlighting key molecular and cellular pathways involved in PE. The review integrates data on oxidative stress biomarkers, angiogenic factors, immune interactions, and mitochondrial dysfunction. PE is initiated by poor placentation due to inadequate trophoblast invasion and improper spiral artery remodeling, leading to placental hypoxia. This triggers the release of anti-angiogenic factors such as soluble fms-like tyrosine kinase-1 (sFlt-1) and soluble endoglin (sEng), causing widespread endothelial dysfunction and systemic inflammation. Oxidative stress, mitochondrial abnormalities, and immune dysregulation further exacerbate the condition. Genetic and epigenetic modifications, including polymorphisms in the Fms-like tyrosine kinase 1 (FLT1) gene and altered microRNA (miRNA) expression, play critical roles. Emerging therapeutic strategies targeting oxidative stress, inflammation, angiogenesis, and specific molecular pathways like the heme oxygenase-1/carbon monoxide (HO-1/CO) and cystathionine gamma-lyase/hydrogen sulfide (CSE/H2S) pathways show promise in mitigating preeclampsia's effects. PE is a complex disorder with multifactorial origins involving abnormal placentation, endothelial dysfunction, systemic inflammation, and oxidative stress. Despite advances in understanding its pathophysiology, effective prevention and treatment strategies remain limited. Continued research is essential to develop targeted therapies that can improve outcomes for both mothers and their babies.
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