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Disruption of the Mouse Blood-Brain Barrier by Small Extracellular Vesicles from Hypoxic Human Placentas
Published on: January 26, 2024
[Nitric oxide and preeclampsia].
1Semmelweis Egyetem, Általános Orvostudományi Kar Orvosi Vegytani Molekuláris Biológiai és Patobiokémiai Intézet, Tűzoltó u. 37-47, Budapest. zoltan.kukor@eok.sote.hu
Orvosi Hetilap
|December 15, 2010
Summary
Preeclampsia pathogenesis involves placental endothelial nitric oxide synthase (eNOS) dysfunction. Factors like substrate deficiency and increased inhibitors impair NO synthesis, contributing to this pregnancy disorder.
Area of Science:
- Obstetrics and Gynecology
- Vascular Biology
- Biochemistry
Context:
- Preeclampsia is a major cause of maternal morbidity and mortality.
- The placenta plays a critical role in preeclampsia development.
- The exact causes of preeclampsia remain unknown despite extensive research.
Purpose:
- To review the role of endothelial nitric oxide synthesis (eNOS) in preeclampsia.
- To discuss known disturbances in placental eNOS function.
- To explore factors affecting NO production in preeclamptic pregnancies.
Summary:
- Insufficient nitric oxide (NO) synthesis is implicated in preeclampsia pathogenesis.
- Deficiencies in arginine, tetrahydrobiopterin (BH4), or calcium can reduce NO synthesis.
- Increased serum levels of free fatty acids (FFA), asymmetric dimethylarginine, reactive oxygen species, and glucose in preeclampsia can decrease NO production.
- Reduced eNOS affinity for BH4 and increased superoxide production occur in preeclamptic placentas.
- eNOS gene polymorphisms have been tentatively linked to preeclampsia complications.
- Smoking may have a protective role, potentially by lowering FFA and through carbon monoxide (CO) mimicking NO.
Impact:
- Understanding eNOS disturbances aids in identifying preeclampsia mechanisms.
- This review highlights key molecular factors influencing NO bioavailability in preeclampsia.
- Further research into eNOS modulation could offer novel therapeutic targets for preeclampsia.
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