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Platelet‑activating factor (PAF) is a potent phospholipid-derived lipid mediator involved in inflammation, thrombosis, and allergic responses. It is endogenously produced by various cells including platelets, endothelial cells, monocytes/macrophages, and polymorphonuclear leukocytes. PAF acts primarily through the platelet‑activating factor receptor (PAFR), a G-protein coupled receptor present on many cell types. Upon binding to its receptor, PAF triggers signaling cascades that result in platelet aggregation, vasodilation or vasoconstriction depending on context, increased vascular permeability, leukocyte activation and chemotaxis, and the release of inflammatory cytokines such as TNF-alpha and interferon gamma. Elevated levels of PAF are implicated in pathological conditions such as allergic reactions (including rhinitis), sepsis, stroke, myocardial infarction, colitis/inflammatory bowel disease, multiple sclerosis and atherosclerosis[4][6][10]. Structurally it is characterized by an ether-linked alkyl group at the sn‑1 position of glycerol backbone with an acetyl group at sn‑2 and a phosphocholine headgroup at sn‑3[4][7]. There are no approved pharmaceutical products containing exogenous PAF; rather it serves as an endogenous signaling molecule whose effects can be modulated by antagonists.
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