@article{3158131,
    title = "Placental growth factor (PlGF): a key to optimizing fetal growth",
    author = "Vrachnis, Nikolaos and Kalampokas, Emmanouil and Sifakis, Stavros and and Vitoratos, Nikolaos and Kalampokas, Theodoros and Botsis, Demetrios and and Iliodromiti, Zoe",
    journal = "Journal of Maternal-Fetal and Neonatal Medicine",
    year = "2013",
    volume = "26",
    number = "10",
    pages = "995-1002",
    publisher = "TAYLOR & FRANCIS LTD LONDON",
    issn = "1476-7058, 1476-4954",
    doi = "10.3109/14767058.2013.766694",
    keywords = "Angiogenesis; fetal growth; Fms-like tyrosine kinase-1; kinase-inserted
domain receptor; placental growth factor; vascular endothelial growth
factor",
    abstract = "The needs of the uterus and the fetus for the provision of nutrients and
oxygen, supplied by the blood flow, are understandably extremely high,
with the circulatory system playing the most important role in this
action. Abnormal vascular growth and transformation that create a high
vessel resistance network have been associated with various pregnancy
pathologies, including miscarriage, small for gestational age (SGA)
fetuses with or without preeclampsia and intrauterine growth restriction
(IUGR). Placental growth factor (PlGF) has a major role in
vasculogenesis and angiogenesis in human placenta. Low concentrations of
PlGF and high concentrations of its inhibitor-soluble Fms-like tyrosine
kinase-1 (sFlt-1) are linked with impaired angiogenesis and placental
development, leading to the above pregnancy complications. The activity
of vascular endothelial growth factor (VEGF), which is the most potent
of all angiogenic mediators, is partly modulated by PlGF. Although the
mechanisms via which PlGF exerts its various effects are still under
investigation, we herein discuss the known actions exerted by this major
mediator together with its results on fetal growth."
}