sFlt-1 (soluble Flt-1) potently inhibits angiogenesis by binding extracellularly to VEGF (vascular endothelial growth factor). In the present paper, we report that hypoxia down-regulates sFlt-1 expression in HMVECs (human microvascular endothelial cells), a constituent of microvessels where angiogenesis occurs. Hypoxia (5-1% O₂) increased VEGF expression in HMVECs. In contrast, the levels of sF...

Elevated expression of soluble vascular endothelial growth factor receptor-1 (sFlt-1) in preeclampsia plays a major role in the pathogenesis of this serious disorder of human pregnancy. Although reduced placental oxygenation is thought to be involved in the pathogenesis of preeclampsia, it is unclear how oxygen regulates placental sFlt-1 expression. The aims herein were to investigate sFlt-1 ex...

Anti‑angiogenesis gene therapy has attracted interest as a potential treatment for hepatocellular carcinoma (HCC). Studies have indicated that soluble fms‑like tyrosine kinase‑1 (sFlt‑1) may suppress angiogenesis by sequestering free vascular endothelial growth factor (VEGF) or by forming inactive heterodimers with VEGF receptor‑2. Mesenchymal stem cells (MSCs) have been widely used as prospect...

BACKGROUND The relationship between fms-like tyrosine kinase-1 (sFlt-1), a soluble receptor for vascular endothelial growth factor (VEGF), and vascular disease has not been established, so this study aimed to elucidate the association between sFlt-1 and the progression of carotid intima - media thickness (IMT) in hypertensive patients. METHODS AND RESULTS The 120 hypertensive patients under m...

Epidemiological studies have shown that maternal preeclampsia (PE) increases the risk of bronchopulmonary dysplasia (BPD), but the underlying mechanism is unknown. Soluble vascular endothelial growth factor receptor-1 (soluble VEGFR1, known as soluble fms-like tyrosine kinase 1, or sFlt-1), an endogenous antagonist of vascular endothelial growth factor (VEGF), is markedly elevated in amniotic f...

RATIONALE Preeclampsia is a devastating medical complication of pregnancy which leads to maternal and fetal morbidity and mortality. While the etiology of preeclampsia is unclear, human and animal studies suggest that excessive circulating levels of soluble fms-like tyrosine-kinase-1 (sFlt-1), an alternatively spliced variant of VEGF-receptor1, contribute to the signs and symptoms of preeclamps...

While soluble fms-like tyrosine kinase-1 (sFlt-1) and endothelin-1 (ET-1) have been implicated in the pathogenesis of preeclampsia (PE), the mechanisms whereby increased sFlt-1 leads to enhanced ET-1 production and hypertension remain unclear. It is well documented that nitric oxide (NO) production is reduced in PE; however, whether a reduction in NO synthesis plays a role in increasing ET-1 an...

OBJECTIVE To examine the distribution of maternal serum soluble fms-like tyrosine kinase-1 (sFlt-1) at 12, 22, 32 and 36 weeks' gestation in singleton pregnancies that develop pre-eclampsia (PE) and examine the performance of this biomarker in screening for PE. METHODS Serum sFlt-1 was measured in 7066 cases at 11-13 weeks, 8079 cases at 19-24 weeks, 8472 at 30-34 weeks and 4043 at 35-37 week...

Preeclampsia as one of the manifestations placental dysfunction associated with dysregulation pro- and antiangiogenic factors. During normal pregnancy, concentration factor sFlt-1 remains low, which allows accurate transmission signals induced by proangiogenic factors VEGF PlGF. This balance is crucial to maintain physiological vasodilation. Under hypoperfusion, placenta increases synthesis sFl...

The balance between proangiogenic and antiangiogenic factors, such as vascular endothelial growth factor, placental growth factor, and soluble fms-like tyrosine kinase-1 (sFlt-1), is altered in preeclampsia, and this dysregulation of angiogenic factors may be important in the pathogenesis of preeclampsia. Although sFlt-1 is elevated in preeclampsia, the mechanisms responsible for increasing thi...