ArticleFrontiers in endocrinology2019
Human sFLT1 Leads to Severe Changes in Placental Differentiation and Vascularization in a Transgenic hsFLT1/rtTA FGR Mouse Model.
Article in Frontiers in endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 36 citations in OpenAlex.
- Aberrant Uteroplacental and Vascular Signaling and Remodeling by Matrix Metalloproteinases in Pregnancy-Related Hypertension and Preeclampsia.Biomolecules · 2026Review
- Ultrasound Microvessel Imaging of the Human Placenta Demonstrates Altered Vessel Densities in Fetal Growth Restriction With Vascular and Immune Pathologies: A Pilot Case-Control Study.Journal of ultrasound in medicine : official journal of the American Institute of Ultrasound in Medicine · 2025Article
- Overexpression of Human sFLT1 in the Spongiotrophoblast Is Sufficient to Induce Placental Dysfunction and Fetal Growth Restriction in Transgenic Mice.International journal of molecular sciences · 2024Article
- Gestational ozone inhalation elicits maternal cardiac dysfunction and transcriptional changes to placental pericytes and endothelial cells.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
- The pathogenesis of obstetric APS: a 2023 update.Clinical immunology (Orlando, Fla.) · 2023Review
- Placental syndromes and maternal cardiovascular health.Clinical science (London, England : 1979) · 2023Review
- Three-Dimensional Histological Characterization of the Placental Vasculature Using Light Sheet Microscopy.Biomolecules · 2023Article
- First-trimester plasma extracellular heat shock proteins levels and risk of preeclampsia.Journal of cellular and molecular medicine · 2023Article
- Growth-Restricted Fetuses and Offspring Reveal Adverse Sex-Specific Metabolic Responses in Preeclamptic Mice Expressing Human sFLT1.International journal of molecular sciences · 2023Article
- Animal Models of Cardiovascular Complications of Pregnancy.Circulation research · 2022Review
- Course of the sFlt-1/PlGF ratio in fetal growth restriction and correlation with biometric measurements, feto-maternal Doppler parameters and time to delivery.Archives of gynecology and obstetrics · 2022Article
- Imbalances in circulating angiogenic factors in the pathophysiology of preeclampsia and related disorders.American journal of obstetrics and gynecology · 2022Review
- The Role of Syncytin in Placental Angiogenesis and Fetal Growth.Frontiers in cell and developmental biology · 2022Article
- Reduced expression in preterm birth of sFLT-1 and PlGF with a high sFLT-1/PlGF ratio in extracellular vesicles suggests a potential biomarker.Frontiers in endocrinology · 2022Article
- Systemic Maternal Human sFLT1 Overexpression Leads to an Impaired Foetal Brain Development of Growth-Restricted Foetuses upon Experimental Preeclampsia.Oxidative medicine and cellular longevity · 2022Article
- HIF-1α regulated pathomechanism of low birth weight through angiogenesis factors in placentalF1000Research · 2022Article
- Selection of reliable reference genes for analysis of gene expression in the rat placenta.Molecular and cellular biochemistry · 2021Article
- Disruption of paternal circadian rhythm affects metabolic health in male offspring via nongerm cell factors.Science advances · 2021Article
- Hypoxia and Mitochondrial Dysfunction in Pregnancy Complications.Antioxidants (Basel, Switzerland) · 2021Review
- Pre-eclampsia Complicated With Maternal Renal Dysfunction Is Associated With Poor Neurological Development at 3 Years Old in Children Born Before 34 Weeks of Gestation.Frontiers in pediatrics · 2021Article
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Authors and funding
12 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The anti-angiogenic soluble fms-like tyrosine kinase 1 (sFLT1) is one of the candidates in the progression of preeclampsia, often associated with fetal growth restriction (FGR). Therapeutic agents against preeclampsia with/without FGR, as well as adequate transgenic sFLT1 mouse models for testing such agents, are still missing. Much is known about sFLT1-mediated endothelial dysfunction in several tissues; however, the influence of sFLT1 on placental and fetal development is currently unknown. We hypothesize that sFLT1 is involved in the progression of FGR by influencing placental differentiation and vascularization and is a prime candidate for interventional strategies. Therefore, we generated transgenic inducible human sFLT1/reverse tetracycline-controlled transactivator (hsFLT1/rtTA) mice, in which hsFLT1 is ubiquitously overexpressed during pregnancy in dams and according to the genetics in hsFLT1/rtTA homozygous and heterozygous fetuses. Induction of hsFLT1 led to elevated hsFLT1 levels in the serum of dams and on mRNA level in all placentas and hetero-/homozygous fetuses, resulting in FGR in all fetuses at term. The strongest effects in respect to FGR were observed in the hsFLT1/rtTA homozygous fetuses, which exhibited the highest hsFLT1 levels. Only fetal hsFLT1 expression led to impaired placental morphology characterized by reduced placental efficiency, enlarged maternal sinusoids, reduced fetal capillaries, and impaired labyrinthine differentiation, associated with increased apoptosis. Besides impaired placental vascularization, the expression of several transporter systems, such as glucose transporter 1 and 3 (
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