Which of the following correctly describes the mechanism by which elevated sFlt-1 causes endothelial dysfunction in pre-eclampsia?
- A sFlt-1 directly activates thromboxane A2 synthesis in trophoblasts
- B sFlt-1 sequesters free circulating VEGF and PlGF, preventing their binding to endothelial receptors ✓
- C sFlt-1 inhibits nitric oxide synthase activity in placental villi
- D sFlt-1 upregulates angiotensin-1 receptor autoantibody production
Correct answer: B. sFlt-1 sequesters free circulating VEGF and PlGF, preventing their binding to endothelial receptors
Explanation
Soluble fms-like tyrosine kinase-1 (sFlt-1) is a truncated, soluble form of the VEGF receptor that circulates in plasma and acts as a decoy receptor, binding and neutralising free VEGF and PlGF before they can engage their endothelial-bound receptors. This reduces endothelial NO production and prostacyclin synthesis, leading to vasoconstriction, proteinuria, and the multi-system features of pre-eclampsia. The other mechanisms are secondary or unrelated.
Reference: Williams Obstetrics, 26th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
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