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Dissecting the soluble Fms-like tyrosine kinase-1/galectin-1 – axis in maternal immune activation related to preeclampsia
Preeclampsia (PE) significantly increases the risk of cardiovascular and metabolic diseases later in life for both mothers and their children. Our understanding of its pathophysiology, prediction, prevention, and treatment options remain limited due to the heterogeneity of the disease. We seek to unravel the complexities of PE by investigating maternal immune activation and angiogenic signatures across different subtypes in order to enhance predictive accuracy and identify novel intervention targets.
Hypothesis
Team
Prof. Dr. med.
Stefan Verlohren
Principal Investigator
Prof. Dr. rer. nat.
Sandra Blois
Principal Investigator
PD Dr.
Evelyn Huhn
Clinician Scientist
Charlotte Harms
PhD Student
Project-related publications
Giesen EM, Verlohren S, Blois SM. Multi-omic insights of preeclampsia and cardiovascular health outcomes. Nature Comm Med (2025).
Anwar R, Pande A, Singh M, Huang Z, Hallett E, Xie Y, Gellhaus A, Herse F, Nonn O, Gauster M Raskó T, Selbach M, Verlohren S, Staff AC, Dechend R, Pecks U, Blois SM, Hurst LD, Izsvák Z. ERV3-MLT1 provides cis-regulatory elements for human placental functioning and are commonly dysregulated in human-specific preeclampsia. Genome Biology (2025). In Press.
Freitag N. et al. Interfering with Gal-1-mediated angiogenesis contributes to the pathogenesis of preeclampsia. Proc Natl Acad Sci U S A 28, 11451-6. (2013) doi: 10.1073/pnas.1303707110.
Schnabel A. et al. Elevated systemic galectin-1 levels characterize HELLP syndrome. J Reprod Immunol 114, 38-43. (2016) doi: 10.1016/j.jri.2016.02.002.
Boehm-Sturm P. et al. Phenotyping placental oxygenation in Lgals1 deficient mice using 19F MRI. Sci Rep 11, 2126 (2021) doi: 10.1038/s41598-020-80408-9.
Barrientos G. et al. Involvement of galectin-1 in reproduction: past, present and future. Hum Reprod Update 2, 175-193 (2014) doi: 10.1093/humupd/dmt040.
Xie Y. et al. Fetal growth restriction induced by maternal gal-3 deficiency is associated with altered gutplacenta axis. Cell Death Dis 15, 575 (2024) doi: 10.1038/s41419-024-06962-6.
Xie Y. et al. Maternal-derived galectin-1 shapes the placenta niche through Sda terminal glycosylation: Implication for preeclampsia. Proc Natl Acad Sci U S A Nexus 2, 8 (2023) doi: 10.1093/pnasnexus/pgad247.
Zeisler H. et al. Predictive Value of the sFlt-1:PlGF Ratio in Women with Suspected Preeclampsia. N Engl J Med 374, 13-22 (2018) doi: 10.1056/NEJMoa1414838.
Dröge L.A. et al. Prediction of Preeclampsia-Related Adverse Outcomes With the sFlt-1 (Soluble fms-Like Tyrosine Kinase 1)/PlGF (Placental Growth Factor)-Ratio in the Clinical Routine: A Real-World Study. Hypertension 77, 461-471 (2021) doi: 10.1161/HYPERTENSIONAHA.120.15146.
Lorenz-Meyer L.A., Frank L., Sroka D., Busjahn A., Henrich W., Verlohren S. Correlation between placental weight and angiogenic markers sFlt-1 and PlGF in women with preeclampsia and fetal growth restriction. Pregnancy Hypertens 28, 149-155 (2022) doi: 10.1016/j.preghy.2022.04.002.
Kirkgöz K. et al. Placental glycosylation senses the anti-angiogenic milieu induced by human sFLT1 during pregnancy. J Reprod Immunol 164, 104284 (2024) doi: 10.1016/j.jri.2024.104284.