Titre
Feto-placental and coronary endothelial genes implicated in miscarriage, congenital heart disease and stillbirth, a systematic review and meta-analysis.
Type
article
Institution
Externe
Périodique
Auteur(s)
Kalisch-Smith, J.I.
Auteure/Auteur
Ehtisham-Uddin, N.
Auteure/Auteur
Rodriguez-Caro, H.
Auteure/Auteur
Liens vers les personnes
ISSN
1532-3102
Statut éditorial
Publié
Date de publication
2024-10
Volume
156
Première page
55
Dernière page/numéro d’article
66
Peer-reviewed
Oui
Langue
anglais
Notes
Publication types: Journal Article ; Systematic Review ; Meta-Analysis ; Review ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Publication Status: ppublish
Résumé
The first trimester placenta is very rarely investigated for placental vascular formation in developmental or diseased contexts. Defects in placental formation can cause heart defects in the fetus, and vice versa. Determining the causality is therefore difficult as both organs develop concurrently and express many of the same genes. Here, we performed a systematic review to determine feto-placental and coronary endothelial genes implicated in miscarriages, stillbirth and congenital heart defects (CHD) from human genome wide screening studies. 4 single cell RNAseq datasets from human first/early second trimester cardiac and placental samples were queried to generate a list of 1187 endothelial genes. This broad list was cross-referenced with genes implicated in the pregnancy disorders above. 39 papers reported feto-placental and cardiac coronary endothelial genes, totalling 612 variants. Vascular gene variants were attributed to the incidence of miscarriage (8 %), CHD (4 %) and stillbirth (3 %). The most common genes for CHD (NOTCH, DST, FBN1, JAG1, CHD4), miscarriage (COL1A1, HERC1), and stillbirth (AKAP9, MYLK), were involved in blood vessel and cardiac valve formation, with roles in endothelial differentiation, angiogenesis, extracellular matrix signaling, growth factor binding and cell adhesion. NOTCH1, AKAP12, CHD4, LAMC1 and SOS1 showed greater relative risk ratios with CHD. Many of the vascular genes identified were expressed highly in both placental and heart EC populations. Both feto-placental and cardiac vascular genes are likely to result in poor endothelial cell development and function during human pregnancy that leads to higher risk of miscarriage, congenital heart disease and stillbirth.
PID Serval
serval:BIB_4741AF99DE6F
PMID
Date de création
2024-09-20T13:40:44.232Z
Date de création dans IRIS
2025-05-20T14:09:20Z