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Placental growth factor (PlGF) is a secreted protein belonging to the vascular endothelial growth factor (VEGF) family, playing a pivotal role in pathological angiogenesis and inflammation [1, 4]. Among its isoforms, PlGF-2 is distinguished by a 21-amino acid basic insertion that functions as a heparin-binding domain, facilitating interaction with neuropilin-1 and neuropilin-2 co-receptors and the extracellular matrix [2, 8, 12]. While PlGF is largely redundant for normal physiological development and healthy adult vasculature, it is significantly upregulated in conditions such as ischemia, malignancy, and chronic inflammation [1, 9]. This disease-restricted expression profile makes it a valuable therapeutic target and diagnostic biomarker [1, 7]. In obstetrics, low maternal serum levels of PlGF, often measured alongside soluble fms-like tyrosine kinase-1 (sFlt-1), serve as a critical indicator for preeclampsia and fetal growth restriction [5, 11, 15]. In oncology and ophthalmology, PlGF is targeted by agents like aflibercept, which acts as a decoy receptor to inhibit the pro-angiogenic signaling that drives tumor growth and neovascular eye diseases [13, 14].
Decoy receptor (VEGF trap) that sequesters PlGF and VEGF; monoclonal antibody-mediated neutralization of PlGF; inhibition of binding to VEGFR-1 and Neuropilin-1/2 receptors.
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