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First-pass extracted concept

soluble fms-like tyrosine kinase 1

Candidate: concept label1 source documents4 linked claims
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Aliases

sFlt-1, sFlt1

Extracted Explainers

What the tool is doing

The abstract describes sFlt1 as an antagonist of VEGF and PlGF and links excess circulating sFlt1 to endothelial dysfunction and preeclampsia-like features.

Source 1DOIPubMed

What problem it solves

It serves as a mechanistic explanatory factor for how placental signals could drive maternal endothelial dysfunction in preeclampsia.

Source 1DOIPubMed

What it does not solve

The abstract does not present sFlt1 as an engineered tool or a complete explanation of all preeclampsia pathophysiology.

Source 1DOIPubMed

Alternatives

The abstract contrasts sFlt1 with exogenous VEGF and PlGF as factors that can rescue or oppose its effects.

Source 1DOIPubMed

Evidence Snippets

placental soluble fms-like tyrosine kinase 1 (sFlt1), an antagonist of VEGF and placental growth factor (PlGF), is upregulated in preeclampsia
Evidence 1Source 1DOIPubMedprovenance

Supporting Sources

Linked Claims

Claim 1causal modelsupports2003Source 1DOIPubMed

Administration of sFlt1 to pregnant rats induces hypertension, proteinuria, and glomerular endotheliosis, supporting a causal contribution of excess sFlt1 to preeclampsia pathogenesis.

Claim 2disease associationsupports2003Source 1DOIPubMed

Placental sFlt1 is upregulated in preeclampsia and systemic sFlt1 levels are increased in affected patients, falling after delivery.

Claim 3mechanismsupports2003Source 1DOIPubMed

Increased circulating sFlt1 in preeclampsia is associated with decreased free VEGF and PlGF and endothelial dysfunction in vitro, which can be rescued by exogenous VEGF and PlGF.

Claim 4mechanismsupports2003Source 1DOIPubMed

VEGF and PlGF cause microvascular relaxation of rat renal arterioles in vitro, and sFlt1 blocks this relaxation.