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Distinct phenotypes in the preeclamptic-like mouse model induced by adenovirus carrying sFlt1 and recombinant sFlt1 protein.
Eur J Med Res
December 2024
Clinical and Translational Research Center, Shanghai Key Laboratory of Maternal Fetal Medicine, Shanghai Institute of Maternal-Fetal Medicine and Gynecologic Oncology, Shanghai First Maternity and Infant Hospital, School of Medicine, Tongji University, Shanghai, 200092, China.
Background: Preeclampsia (PE) is a pregnancy-specific, multisystemic disorder that affects 2-8% pregnancies worldwide and is a leading cause of maternal and perinatal mortality. At present, there is no cure for PE apart from delivery the placenta. Therefore, it is important and urgent to possess a suitable animal model to study the pathology and treatment of PE.
View Article and Find Full Text PDFRole of Decidual Natural Killer Cells in the Pathogenesis of Preeclampsia.
Am J Reprod Immunol
January 2025
Department of Obstetrics and Gynecology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Preeclampsia is one of the most severe obstetric complications, yet its pathogenesis remains unclear. Decidual natural killer (dNK) cells, the most abundant immune cells at the maternal-fetal interface, are closely associated with preeclampsia due to abnormalities in their quantity, phenotype, and function. This review summarizes the molecular mechanisms by which dNK cells regulate extravillous trophoblast (EVT) invasion, promote uterine spiral artery remodeling, and maintain immune tolerance.
View Article and Find Full Text PDFDistinct gut microbial signature and altered short chain fatty acid metabolism at disease onset in a rat preclinical model of superimposed preeclampsia.
Sci Rep
December 2024
Laboratorio de Medicina Experimental, Hospital Alemán, Av. Pueyrredón 1640, C1118AAT, Ciudad Autónoma de Buenos Aires, Argentina.
Chronic hypertension is an increasingly prevalent condition that constitutes a risk factor for superimposed preeclampsia during pregnancy. In this study, we assessed the gut microbiome in a rat model of superimposed preeclampsia to characterize the microbial signature associated with defective placentation processes identified at the preclinical disease stage. The blood pressure profile, renal function parameters and fetal phenotype were evaluated in pregnant Stroke-prone Spontaneously Hypertensive Rats (SHRSP) and their normotensive controls.
View Article and Find Full Text PDFCirculating extracellular vesicles and neutrophil extracellular traps contribute to endothelial dysfunction in preeclampsia.
Front Immunol
December 2024
Barcelona Endothelium Team, Hospital Clínic de Barcelona, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), Barcelona, Spain.
Background: Preeclampsia (PE) is a pregnancy complication characterized by hypertension, proteinuria, endothelial dysfunction, and complement dysregulation. Placenta-derived extracellular vesicles (EVs), necessary in maternal-fetal communication, might contribute to PE pathogenesis. Moreover, neutrophil extracellular traps (NETs) play a pathogenic role in other complement-mediated pathologies, and their contribution in PE remains unexplored.
View Article and Find Full Text PDF[Use of hydroxychloroquine in recurrent immune-mediated obstetric diseases (excluding systemic lupus): Scientific basis and evidence].
Rev Med Interne
December 2024
Service de médecine interne et inflammation, département inflammation-immunopathologie-biothérapie (DMU I3), CEREMAIAA, hôpital Saint-Antoine, AP-HP, Sorbonne université, Paris, France.
Hydroxychloroquine (HCQ), a synthetic antimalarial, is recognized for its immunomodulatory, anti-inflammatory and vascular-protective effects. In 20-30% of cases of primary obstetrical antiphospholipid syndrome (APS), the combination of antiplatelet aggregation and prophylactic anticoagulation fails to prevent obstetrical complications, a situation referred to as refractory obstetrical APS. This is partly due to the pro-inflammatory effects of antiphospholipid antibodies (aPL) binding to decidual and trophoblastic cells, which compromise embryonic implantation and placentation.
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