ArticleNature communications2023
Defects in placental syncytiotrophoblast cells are a common cause of developmental heart disease.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 50 citations in OpenAlex.
- The TRAP complex (SSR1-SSR4): mechanistic roles and therapeutic opportunities.Annals of medicine · 2026Review
- Maternal Kisspeptin-10 Treatment Partially Rescues Fetal and Postnatal Cardiac Programming Disrupted by Maternal Hypothyroidism.Cardiovascular toxicology · 2026Article
- Placental Dysfunction and Congenital Heart Disease: Investigating the Placenta-Heart Axis.Prenatal diagnosis · 2026Article
- Diminished Late Gestation Placental Volume in Fetal Heart Disease and Implications for Birth Anthropometrics.Journal of cardiovascular development and disease · 2026Article
- Dll4 assembles the umbilical cord and placental vasculature.JCI insight · 2026Article
- Tim1 Deficiency Mediates Gestational Hyperglycemia-Related Syncytiotrophoblast Dysfunction and Fetal Growth Restriction.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Non-coding RNAs in congenital heart disease and placental development: Bridging molecular mechanisms to clinical biomarkers and therapies.Non-coding RNA research · 2026Review
- Unveiling of Placental-Fetal Heart Interplay: A Novel Etiologic and Therapeutic Insight-A Narrative Review.Journal of pregnancy · 2026Review
- Human fetal circulating factors from pregnancies complicated by obesity upregulate genes associated with pathological hypertrophy in neonatal rat cardiomyocytes.American journal of physiology. Heart and circulatory physiology · 2026Article
- Maternal high-fat, high-sucrose diet-induced excess adiposity is linked to placental hypoxia and disruption of fetoplacental immune homeostasis in late gestation†.Biology of reproduction · 2025Article
- The placental effects of trisomy for human chromosome 21 orthologs in four mouse models of Down syndrome.Biology open · 2025Article
- Placental Malperfusion Is Associated With Adverse Outcomes in Congenital Heart Disease and With Genetic Variants in Placental Developmental Pathways.Journal of the American College of Cardiology · 2025Article
- Mapping the placental galectin-3 interactome identifies CD9 and ITGB1 as functional glycoprotein counterreceptors during syncytialization.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Placental and Fetal Brain Volumes in Congenital Heart Disease Are Smallest Among Fetuses With Genetic Abnormalities.Prenatal diagnosis · 2025Article
- A roadmap towards targeted differentiation of mouse trophoblast stem cells into cell types of the feto-maternal exchange surface.Stem cell research & therapy · 2025Article
- Targeting Decidual CD16Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Feto-placental blood vessel development.Development (Cambridge, England) · 2025Review
- Phospholipid flippase ATP11A brokers uterine epithelial integrity and function.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Single-cell RNA sequencing identifies CXADR as a fate determinant of the placental exchange surface.Nature communications · 2025Article
- Placental histology, perioperative brain development, and neurodevelopmental outcome at 1 year of age in patients undergoing neonatal cardiac surgery-is there an association?Frontiers in cardiovascular medicine · 2025Article
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Placental abnormalities have been sporadically implicated as a source of developmental heart defects. Yet it remains unknown how often the placenta is at the root of congenital heart defects (CHDs), and what the cellular mechanisms are that underpin this connection. Here, we selected three mouse mutant lines, Atp11a, Smg9 and Ssr2, that presented with placental and heart defects in a recent phenotyping screen, resulting in embryonic lethality. To dissect phenotype causality, we generated embryo- and trophoblast-specific conditional knockouts for each of these lines. This was facilitated by the establishment of a new transgenic mouse, Sox2-Flp, that enables the efficient generation of trophoblast-specific conditional knockouts. We demonstrate a strictly trophoblast-driven cause of the CHD and embryonic lethality in one of the three lines (Atp11a) and a significant contribution of the placenta to the embryonic phenotypes in another line (Smg9). Importantly, our data reveal defects in the maternal blood-facing syncytiotrophoblast layer as a shared pathology in placentally induced CHD models. This study highlights the placenta as a significant source of developmental heart disorders, insights that will transform our understanding of the vast number of unexplained congenital heart defects.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.