Gene polymorphism associated with <i><scp>TGF</scp>‐β1</i> and susceptibility to preeclampsia: A meta‐analysis and trial sequential analysis

Liu, Jing; Song, Guang; Zhao, Ge; Meng, Ting

doi:10.1111/jog.14751

Cited by 5 publications

(3 citation statements)

References 31 publications

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“…There are multiple maternal and fetal gene alleles and mutations associated with pre-eclampsia [33][34][35][36][37][38][39] , possibly reflecting the syndromic nature of this disease. Many of these identified genes are associated with thrombophilic factors [34][35][36][37] , angiogenic factors 33,40 or immune responses 38,39 . Fetal trisomy 13 is also associated with increased risk of pre-eclampsia likely due to the extra copy of FLT1 (encoding Fms-related receptor tyrosine kinase 1; FLT1), which is located on chromosome 13 (ref.…”

Section: Genetic Risk Factorsmentioning

confidence: 99%

Pre-eclampsia

Dimitriadis

Rolnik

Zhou

et al. 2023

Nat Rev Dis Primers

198

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Pre-eclampsia is a life-threatening disease of pregnancy unique to humans and a leading cause of maternal and neonatal morbidity and mortality. Women who survive pre-eclampsia have reduced life expectancy, with increased risks of stroke, cardiovascular disease and diabetes, while babies from a pre-eclamptic pregnancy have increased risks of preterm birth, perinatal death and neurodevelopmental disability and cardiovascular and metabolic disease later in life. Preeclampsia is a complex multisystem disease, diagnosed by sudden-onset hypertension (>20 weeks of gestation) and at least one other associated complication, including proteinuria, maternal organ dysfunction or uteroplacental dysfunction. Pre-eclampsia is found only when a placenta is or was recently present and is classified as preterm (delivery <37 weeks of gestation), term (delivery ≥37 weeks of gestation) and postpartum pre-eclampsia. The maternal syndrome of pre-eclampsia is driven by a dysfunctional placenta, which releases factors into maternal blood causing systemic inflammation and widespread maternal endothelial dysfunction. Available treatments target maternal hypertension and seizures, but the only 'cure' for pre-eclampsia is delivery of the dysfunctional placenta and baby, often prematurely. Despite decades of research, the aetiology of pre-eclampsia, particularly of term and postpartum pre-eclampsia, remains poorly defined. Significant advances have been made in the prediction and prevention of preterm pre-eclampsia, which is predicted in early pregnancy through combined screening and is prevented with daily low-dose aspirin, starting before 16 weeks of gestation. By contrast, the prediction of term and postpartum pre-eclampsia is limited and there are no preventive treatments. Future research must investigate the pathogenesis of pre-eclampsia, in particular of term and postpartum pre-eclampsia, and evaluate new Nature Reviews Disease Primers | (2023) 9:8 2 0123456789();: Primer Epidemiology Incidence and mortalityThe global prevalence of all pre-eclampsia in the years 2002-2010 was estimated at 4.6% of deliveries but reported regional rates varied between 1% and 5.6% 14 . Where reported, the prevalence of preterm pre-eclampsia is <1% [15][16][17][18] . The prevalence of pre-eclampsia is generally reported as lower in low-income and middle-income countries (LMICs) (except sub-Saharan Africa) than in high-income countries (HICs) 19,20 ; however, it is likely that differences in classification, access to prenatal care and under-reporting in LMICs affect prevalence data 20,21 . Furthermore, most pre-eclampsia research is performed in HICs, potentially leading to bias and generalizability concerns in the populations sampled and the research questions asked.Hypertensive disorders of pregnancy (including pre-eclampsia) are the second most common cause (behind haemorrhage) of maternal Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rights...

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Section: Genetic Risk Factorsmentioning

confidence: 99%

Pre-eclampsia

Dimitriadis

Rolnik

Zhou

et al. 2023

Nat Rev Dis Primers

198

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“…There are only a few studies utilizing WGCNA in the analysis of genetic predispositions toward preeclampsia. The majority of the studies in this field mainly identify gene polymorphisms in various population groups [ 39 , 40 , 41 , 42 ]. We reiterate that WGCNA might be a more suitable analysis compared to the analysis of differential expression of genes for a broader look into the networks responsible for the pathophysiology of the disease.…”

Section: Discussionmentioning

confidence: 99%

G-Protein Coupled Receptor Dysregulation May Play Roles in Severe Preeclampsia—A Weighted Gene Correlation Network Analysis of Placental Gene Expression Profile

Vidal

Deguit

et al. 2022

Cells

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Preeclampsia is one of the major hypertensive diseases of pregnancy. Genetic factors contribute to abnormal placentation. The inadequate transformation of cytotrophoblasts causes failure of maternal spiral arteries’ remodeling and results in narrow, atherotic-prone vessels, leading to relative placental ischemia. This study aims to explore the possibility of identifying dysregulated gene networks that may offer a potential target in the possible prevention of preeclampsia. We performed a weighted gene correlated network analysis (WGCNA) on a subset of gene expression profiles of placental tissues from severe preeclamptic pregnancies. We identified a gene module (number of genes = 402, GS = 0.35, p = 0.02) enriched for several G-protein-coupled receptor (GPCR)-related genes with significant protein–protein molecular interaction (number of genes = 38, FDR = 0.0007) that may play key roles in preeclampsia. Some genes are noted to play key roles in preeclampsia, including LPAR4/5, CRLR, NPY, TACR1/2, and SFRP4/5, whose functions generally relate to angiogenesis and vasodilation or vasoconstriction. Other upregulated genes, including olfactory and orexigenic genes, serve limited functions in the disease pathogenesis. Altogether, this study shows the utility of WGCNA in exploring possible new gene targets, and additionally reinforces the feasibility of targeting GPCRs that may offer intervention against development and disease progression among severe preeclampsia patients.

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“…Gannoun et al investigated genetic polymorphisms in the promoter region of matrix metalloproteinases 9 and 2 (MMP-9 and -2) in a Tunisian Arab population and revealed that the MMP-9 rs3918242 (-562 C > T) variant is related to increased MMP-9 production and is a risk factor for PE [ 90 ]. In a recently published meta-analysis, Liu et al identified transforming growth factor-beta 1(TGF-β1) rs800469 variant as a possible risk factor for PE in Asian population [ 91 ]. TGF-β1 is a cytokine produced during pregnancy by trophoblast cells, involved in the regulation of trophoblast proliferation, differentiation and invasion.…”

Section: Fetal Growth Restriction and Preeclampsia As A Maternal Factormentioning

confidence: 99%

Genetic Background of Fetal Growth Restriction

Nowakowska¹,

Pankiewicz²,

Nowacka³

et al. 2021

IJMS

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Fetal growth restriction (FGR) is one of the most formidable challenges in present-day antenatal care. Pathological fetal growth is a well-known factor of not only in utero demise in the third trimester, but also postnatal morbidity and unfavorable developmental outcomes, including long-term sequalae such as metabolic diseases, diabetic mellitus or hypertension. In this review, the authors present the current state of knowledge about the genetic disturbances responsible for FGR diagnosis, divided into fetal, placental and maternal causes (including preeclampsia), as well as their impact on prenatal diagnostics, with particular attention on chromosomal microarray (CMA) and noninvasive prenatal testing technique (NIPT).

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Gene polymorphism associated with TGF‐β1 and susceptibility to preeclampsia: A meta‐analysis and trial sequential analysis

Cited by 5 publications

References 31 publications

Pre-eclampsia

Pre-eclampsia

G-Protein Coupled Receptor Dysregulation May Play Roles in Severe Preeclampsia—A Weighted Gene Correlation Network Analysis of Placental Gene Expression Profile

Genetic Background of Fetal Growth Restriction

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