The role of thrombophilias and angiogenic factors in the pathogenesis of fetal growth retardation syndrome
The review discusses the role of the possible etiopathogenic factors of fetal growth retardation syndrome such as the genetic forms of thrombophilias and angiogenic growth factors. The most common genetic defects of hemostasis leading to the development of FGRS are resistance to activated protein C (APC), the factor V Leiden mutation, prothrombin G20210A mutation, congenital deficiencies of С and S protein, antithrombin III deficiency, defects of plasminogen tissue activator and plasminogen activator inhibitor (PAI). In the past decades, researchers of FGRS and PI have paid attention to these risk factors and their receptors. Of much interest are the vascular-endothelial growth factor (FEGF), the placenta growth factor (PGF), and also their receptor possessing thyrosine kinase activity (VEGF-R or Flt-1 or VEGFR-1), the insulin-like growth factor (IGF) is of special importance.