Maternal/fetal eNOS-<i>Glu298Asp</i> genotypes and their influence on the severity, prognosis, and lipid profile of preeclampsia

Procopciuc, Lucia Maria; Caracostea, Gabriela; Hazi, Georgeta; Nemeti, Georgiana; Zaharie, Gabriela; Stamatian, Florin

doi:10.1080/14767058.2017.1323329

Cited by 7 publications

(4 citation statements)

References 27 publications

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“…In our BNM analyses, we blocklisted potential edges from offspring SNPs to maternal phenotypes and fasting/1-hr maternal metabolites such that no such edge could be included in the estimated models. However, there is evidence that offspring genotype can have limited influence maternal phenotypes [31,32]. Implementing the specified blocklist prevented the discovery of such rare occurrences with our data.…”

Section: Discussionmentioning

confidence: 75%

Network Approaches to Integrate Analyses of Genetics and Metabolomics Data with Applications to Fetal Programming Studies

et al. 2022

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The integration of genetics and metabolomics data demands careful accounting of complex dependencies, particularly when modelling familial omics data, e.g., to study fetal programming of related maternal–offspring phenotypes. Efforts to identify genetically determined metabotypes using classic genome wide association approaches have proven useful for characterizing complex disease, but conclusions are often limited to a series of variant–metabolite associations. We adapt Bayesian network models to integrate metabotypes with maternal–offspring genetic dependencies and metabolic profile correlations in order to investigate mechanisms underlying maternal–offspring phenotypic associations. Using data from the multiethnic Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study, we demonstrate that the strategic specification of ordered dependencies, pre-filtering of candidate metabotypes, incorporation of metabolite dependencies, and penalized network estimation methods clarify potential mechanisms for fetal programming of newborn adiposity and metabolic outcomes. The exploration of Bayesian network growth over a range of penalty parameters, coupled with interactive plotting, facilitate the interpretation of network edges. These methods are broadly applicable to integration of diverse omics data for related individuals.

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Section: Discussionmentioning

confidence: 75%

Network Approaches to Integrate Analyses of Genetics and Metabolomics Data with Applications to Fetal Programming Studies

et al. 2022

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“…Any change occurring in this gene can affect the production of NO, which can lead to hypertension, coronary artery disorder, and PE. Furthermore, another study reported the SNP polymorphism in eNOS, also caused endothelial dysfunction, which can increase oxidative stress [ 10 ]. Another study performed on the Turkish population indicated that eNOS gene (Glu298Asp) polymorphism was more prevalent in PE patients and may lead to eclampsia [ 103 ].…”

Section: Genetic Polymorphism and Its Association With Pre-eclampsiamentioning

confidence: 99%

“…[ 9 ]. Furthermore, many maternal, fetal, environmental and genetic risk factors are involved in the development of PE [ 10 ].…”

Section: Introductionmentioning

confidence: 99%

Pre-Existing Diabetes Mellitus, Hypertension and KidneyDisease as Risk Factors of Pre-Eclampsia: A Disease of Theories and Its Association with Genetic Polymorphism

Alanazi

Victor

Rehman

et al. 2022

IJERPH

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Pre-existing diabetes, hypertension and kidney disorders are prominent risk factors of pre-eclampsia (PE). It is a multifactorial pregnancy disorder associated with high blood pressure, proteinuria, and multiorgan failure, which develops after the 20th week of pregnancy. It is one of the most feared pregnancy disorders, as it consumes thousands of fetomaternal lives per annum. According to clinical and pathological studies, the placenta appears to be a key player in the pathogenesis of PE; however, the exact origin of this disorder is still under debate. Defective placentation and angiogenesis are the hallmarks of PE progression. This angiogenic imbalance, together with maternal susceptibility, might determine the severity and clinical presentation of PE. This article comprehensively examines the mechanisms of pathogenesis of PE and current evidence of the factors involved in its progression. Finally, this article will explore the genetic association of PE, various candidate genes, their proposed mechanisms and variants involved in its pathogenesis.

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“…Similarly, higher lipid concentrations are seen in newborns, which could be associated with a risk of dyslipidamia in adulthood [ 53 ]. In this context, newborns of mothers who have PE, due to dysregulation in the production of or damage to key molecules required for a healthy foetal environment, are at risk of neurological diseases; disabilities such as cerebral palsy, retardation, sensory deficiencies or behaviour disorders; metabolic diseases such as diabetes, hypertension, metabolic syndrome, and dyslipidaemia; and cardiovascular diseases such as coronary heart disease, cerebrovascular disease, and peripheral vascular disease [ 54 , 55 ].…”

Section: Introductionmentioning

confidence: 99%

Foetal lipoprotein oxidation and preeclampsia

2022

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Preeclampsia (PE) is a multisystemic syndrome specific to pregnancy. Although PE is the leading cause of death from complications associated with pregnancy, its aetiology is still unknown. In PE, lipid metabolism is altered. When lipids are damaged, both the mother and the foetus may be at risk. Lipoproteins contain apolipoproteins, triacylglycerols, free and esterified cholesterol, and phospholipids, all of which are susceptible to oxidative stress when high levels of oxygen and nitrogen free radicals are present. Lipoperoxidation can occur in three stages: mild, moderate, and severe. In severe lipid damage, highly toxic products such as malondialdehyde (MDA) can be generated; under these conditions, low-density lipoprotein (LDL) proteins can be oxidized (oxLDL). oxLDL is a biomolecule that can affect the production of nitric oxide (NO), the main vasodilator derived from the endothelium. oxLDL can interfere with the transduction of the signals responsible for triggering the activation of endothelial nitric oxide synthase (eNOS), causing reduced vasodilation and endothelial dysfunction, which are the main characteristics of preeclampsia. The objective of the review was to analyse the information the current information about exists about the impact generated by the oxidation of LDL and HDL lipoproteins in neonates of women with preeclampsia and how these alterations can predispose the neonate to develop diseases in adulthood.PE can cause foetal loss, intrauterine growth restriction, or developmental complications. Neonates of mothers with PE have a high risk of cardiovascular diseases, stroke, mental retardation, sensory deficiencies and an increased risk of developing metabolic diseases. PE not only affects the foetus, generating complications during pregnancy but also predisposes them to chronic diseases in adulthood.

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Maternal/fetal eNOS-Glu298Asp genotypes and their influence on the severity, prognosis, and lipid profile of preeclampsia

Abstract: The eNOS-Glu298Asp variant (in mothers and newborns) in association with dyslipidemia could affect bioavailability of NO and could represent an increased risk for preeclampsia.

Cited by 7 publications

References 27 publications

Network Approaches to Integrate Analyses of Genetics and Metabolomics Data with Applications to Fetal Programming Studies

Network Approaches to Integrate Analyses of Genetics and Metabolomics Data with Applications to Fetal Programming Studies

Pre-Existing Diabetes Mellitus, Hypertension and KidneyDisease as Risk Factors of Pre-Eclampsia: A Disease of Theories and Its Association with Genetic Polymorphism

Foetal lipoprotein oxidation and preeclampsia

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