Excess placental soluble fms-like tyrosine kinase 1 (sFlt1) could contribute to endothelial dysfunction, hypertension, and proteinuria in preeclampsia

By S. Maynard, J. Min, J. Merchan, K. Lim, Jianyi Li, S. Mondal, T. Libermann, James P. Morgon, F. Sellke, I. Stillman and 3 more. 2003

1,515 citations recorded by the source corpus.

Subfields: Cancer Research, Obstetrics and Gynecology, Pediatrics, Perinatology and Child Health

View Paper: https://www.semanticscholar.org/paper/9c295c24a5389737948b5a9b21cfe5e32aa99db0

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cancer Research

1. Seppo Ylä-Herttuala
2. L. Claesson‐Welsh
3. R. Khalil
4. S. Bhardwaj
5. M. Shibuya
6. H. Roy

In Obstetrics and Gynecology

1. M. Shibuya
2. Roberto Romero
3. T. Chaiworapongsa

In Pediatrics, Perinatology and Child Health

1. M. Shibuya

Citations in the corpus

• Trophoblast differentiation during embryo implantation and formation of the maternal-fetal interface. (2004, background): “discovery that excess sFlt-1 produces a preeclampsia-like syndrome in rats (123).”
• Vascular endothelial growth factor and its receptor system: physiological functions in angiogenesis and pathological roles in various diseases. (2013, methodology): “In 2003–2004, several researchers reported that an abnormal increase in the level of serum sFlt-1 in pregnant mothers is well correlated with the degree of PE (38-40) (Fig.”
• Endogenous VEGF Is Required for Visual Function: Evidence for a Survival Role on Müller Cells and Photoreceptors (2008, background): “Similarly, preeclampsia, which is mediated in part by elevated circulating levels of a soluble form of VEGF receptor 1 called sFlt1 leading to systemic VEGF neutralization [25], is also associated with ocular symptoms including RPE lesions, choroidal ischemia and retinal detachments [26,27].”
• Soluble endoglin contributes to the pathogenesis of preeclampsia (2006, background): “We and others recently showed that high levels of circulating sFlt1 (soluble fms-like tyrosine kinase, also known as soluble VEGF receptor 1) of placental origin may contribute to the pathogenesis of preeclampsi”
• Global mapping of binding sites for Nrf2 identifies novel targets in cell survival response through ChIP-Seq profiling and network analysis (2010, background): “For example, Nrf2 target gene, Pdgf is involved in a prenatal placental disorder, preeclampsia, because of increasing levels of their antagonist, fms-like tyrosine kinase 1 (Flt1) (58,59).”
• Pathophysiology of hypertension during preeclampsia linking placental ischemia with endothelial dysfunction. (2001, background): “Considerable clinical evidence has accumulated that preeclampsia is strongly linked to an imbalance between proangiogenic (VEGF and PlGF) and antiangiogenic (sFlt-1) factors in the maternal circulation (47, 50, 51, 66, 74, 93, 103, 104, 117).”
• Biology of vascular endothelial growth factors (2006, background): “A soluble form of VEGFR-1 (sVEGFR-1), consisting of the extracellular domain of VEGFR-1, is able to inhibit VEGF action in humans and mice and has been linked to preeclampsia [43].”
• A longitudinal study of angiogenic (placental growth factor) and anti-angiogenic (soluble endoglin and soluble vascular endothelial growth factor receptor-1) factors in normal pregnancy and patients destined to develop preeclampsia and deliver a small for gestational age neonate (2008, background): “[16] reported the central observation that sVEGFR-1 participates in the pathophysiology of PE, and Levine et al.”
• Signal transduction by vascular endothelial growth factor receptors. (2012, background): “Moreover, sFlt1 is expressed in the placenta in a regulated manner during gestation (Clark et al. 1998) and has been implicated in the pathogenesis of preeclampsia (Maynard et al. 2003).”
• Risk Factors Associated with Acute Pyelonephritis in Healthy Women (2005, methodology): “Analysis of previous work revealed no significant differences in maternal serum sFlt1 or PlGF concentrations according to infant sex.(5,6) Of the 4589 women enrolled in the CPEP trial, we excluded 253 who were lost to follow-up, 21 whose pregnancy ended before 20 weeks, 13 who had missing data on ma”