Briones VCG, Meneses CJ, Moreno SAA, González DJI, Díaz de León PMA, Carlos Briones GJ

Language: Spanish
References: 21
Page: 99-104
PDF size: 88.46 Kb.

ABSTRACT

Preeclampsia is the first cause of maternal death in Mexico. The pathogenic key factor in this disease is the endothelial dysfunction. Recently, several studies have reported that endogline and soluble fms-like tyrosine kinase 1 (sFlt-1), both antiangiogenic proteins, are increased in the placenta and serum of women with preeclampsia. The sFlt-1 (antiangiogenic protein) acts by adhering to the receptor-binding domains of placental growth factor (PlGF) and vascular endothelial growth factor (VEGF), preventing their interaction with endothelial receptors on the cell surface and thereby inducing endothelial dysfunction. Decreased concentrations of circulating free PlGF and free VEGF have been noted during clinical preeclampsia. Excess of sFlt-1 and endogline (antiangiogenic proteins) and the decrease of PlGF and VEGF (angiogenic proteins) may have an important pathogenic role in preeclampsia.

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