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Endothelial Nitric Oxide synthase (eNOS) in Preeclampsia: An Update
Rebecca Ssengonzi1, Yuye Wang1, Nobuyo Maeda-Smithies1
1Department of Pathology and Laboratory Medicine, The University of North Carolina, Chapel Hill, NC 27599, USA.
Insights
Preeclampsia, a pregnancy disorder, is linked to genetic factors like eNOS. Research explores how manipulating the eNOS/NO pathway may help treat this condition and reduce risks for mothers and infants.
Area of Science:
- Obstetrics and Gynecology
- Cardiovascular Research
- Genetics
Background:
- Preeclampsia (PE) is a major cause of maternal and infant mortality, with increasing incidence and healthcare costs in the US.
- PE poses long-term health risks, including cardiovascular and cerebrovascular diseases, for both mother and child.
- Current treatments for PE are lacking, and its underlying causes remain largely unknown.
Purpose of the Study:
- To review studies investigating the role of endothelial nitric oxide synthase (eNOS) in preeclampsia.
- To explore the potential of manipulating the eNOS/NO pathway for preeclampsia intervention.
Main Methods:
- Review of human epidemiological studies linking genetic factors, specifically eNOS variants, to PE.
- Analysis of animal experimental studies demonstrating a functional connection between eNOS and PE.
- Synthesis of research on eNOS/NO pathway modulation for disease intervention.
Main Results:
- Human studies indicate an association between eNOS gene variants and preeclampsia.
- Animal studies provide evidence for a functional role of eNOS in PE development.
- The eNOS/NO pathway is implicated as a potential therapeutic target for PE.
Conclusions:
- Endothelial nitric oxide synthase (eNOS) plays a significant role in preeclampsia.
- Targeting the eNOS/NO pathway presents a promising avenue for future preeclampsia interventions.
- Further research into the genetic and functional aspects of eNOS in PE is warranted.
Abstract:
Preeclampsia (PE) is a common pregnancy-related hypertensive disorder and is a leading cause of maternal and perinatal morbidity and mortality. The incidence of PE and its associated health care costs have been increasing in the United States over the past three decades. Pregnancies complicated by PE put both the mother and child at increased risk for chronic illnesses such as cardiovascular disease, cerebrovascular disease, and cognitive impairment later in life. To date, there is no effective treatment for PE and the etiology of PE is largely unknown. While human epidemiological studies have established an association between various genetic factors and PE, a causative link between genes associated with PE and PE development has been difficult to establish. Human studies have shown that variants in eNOS (endothelial nitric oxide synthase, also known as NOS3) gene are associated with PE, and animal experimental studies have provided evidence to show the potential functional connection between the eNOS gene and PE. Here we review several studies that investigated the role of eNOS in PE, as well as studies that described how manipulating the eNOS/NO pathway could aid in disease intervention.
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