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Placental growth factor 1 (PlGF-1) is a glycosylated homodimeric protein and a member of the vascular endothelial growth factor (VEGF) family [2, 3]. It is primarily expressed in the placenta, but also in the heart, lungs, and skeletal muscle under pathological conditions such as ischemia or inflammation [1, 3]. PlGF-1 acts as a potent angiogenic and inflammatory mediator by specifically binding to the vascular endothelial growth factor receptor-1 (VEGFR-1/Flt-1), but unlike VEGF-A, it does not bind to VEGFR-2 [1, 5, 8]. In clinical medicine, PlGF-1 is a well-established biomarker for preeclampsia, where abnormally low maternal serum levels indicate impaired placental development and high risk of adverse outcomes [2, 11, 13]. Therapeutically, PlGF is targeted by decoy receptors like aflibercept to treat neovascular age-related macular degeneration and various cancers, as its inhibition suppresses pathological vessel growth and inflammatory cell recruitment [1, 5, 12]. Because PlGF-1 signaling is largely restricted to pathological states, targeting it may offer a more favorable safety profile compared to broad VEGF inhibition [1, 14].
Neutralization of circulating PlGF-1 to prevent its interaction with VEGFR-1 (Flt-1), thereby inhibiting pathological angiogenesis, vascular permeability, and the recruitment of inflammatory cells [1, 5, 12].
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