Angiogenesis, defined as the development of new capillaries from preexisting blood vessels, plays a pivotal role in a number of physiological and pathological conditions like cancer, psoriasis, diabetic retinopathy and chronic inflammatory diseases.Vascular endothelial growth factor (VEGF), a major regulator for angiogenesis, has many biological effects by inducing proliferation and migration and by preventing apoptosis of endothelial cell.VEGF binds and activates two tyrosine kinase receptors, VEGFR1 (Flt-1) and VEGFR2 (KDR/Flk-1).These receptors regulate physiological as well as pathological angiogenesis.VEGFR1 is a member of the VEGFR family, and binds VEGF-A, PIGF, and VEGF-B.VEGFR1 plays dual role, a negative role in angiogenesis in the embryo most likely by trapping VEGF-A in a positive role in adulthood.An important feature of VEGFR1 is that, unlike other VEGFR genes, it express two types of mRNA, one for a full-length receptor and another for a soluble short protein known as soluble VEGFR1(sFlt-1).A soluble truncated form of VEGFR1 (sFlt-l) binds to VEGF as strongly as does full-lenght VEGFR1 and inhibits VEGF activity by sequestering it from signalling receptors and by forming non-signalling heterodimers with VEGFR2.Particularly high levels of sFlt-1 exist in the placenta, where it might control VEGF activity at particular stages of pregnancy.If it occurs abnormally overexpression in pregnancy, it would make a preeclamtic symptoms.We have speculated that sFlt-1 has bear unknown potency control and coordinate in angiogenesis.Such an understanding will be vital in the future design of therapeutic agents to control angiogenesis.