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The phospholipid bilayer of vascular endothelial cell membranes is a complex lipid-protein assembly that serves as the primary barrier between the blood and underlying tissues (Pober & Sessa, 2007). It plays a vital role in vascular homeostasis by regulating selective permeability, leukocyte trafficking, and signal transduction through various membrane-bound receptors (Aird, 2007). In healthy physiological states, the bilayer maintains an asymmetric distribution of phospholipids, with anionic species like phosphatidylserine (PS) restricted to the inner leaflet (Bevers & Williamson, 2016). However, in pathological conditions such as cancer, inflammation, or viral infection, this asymmetry is disrupted, leading to the exposure of PS on the outer surface of the endothelial cells (Gerber et al., 2011). This externalization provides a unique therapeutic window, allowing drugs like Bavituximab to selectively bind to the tumor-associated or infected vasculature and induce immune-mediated destruction. Beyond serving as a docking site for targeted therapies, the physical state of the membrane—including its fluidity and lipid composition—is a target for agents aimed at stabilizing the endothelium in cardiovascular diseases (Escribá et al., 2008).
Binding to externalized anionic phospholipids (e.g., phosphatidylserine) to induce antibody-dependent cellular cytotoxicity (ADCC) or modulating membrane fluidity and permeability to stabilize vascular function.
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