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Scavenger receptor class A (SR-A1, also known as SCARA1 or CD204) is a type II transmembrane glycoprotein that forms homotrimers on cell surfaces, mainly on macrophages but also on endothelial and smooth muscle cells. It has a characteristic collagen-like domain responsible for ligand binding and a scavenger receptor cysteine-rich (SRCR) domain. SR-A1 is a prototype member of the scavenger receptor superfamily and recognizes a wide variety of polyanionic ligands, including modified low-density lipoproteins (acLDL, oxLDL), heat shock proteins, bacterial components, and amyloid-β. It is heavily implicated in atherogenesis (through foam cell formation), innate immune defense (by mediating bacterial and viral uptake), regulation of apoptosis, and modulating inflammatory responses. Dysregulation or overexpression of SR-A1 is associated with increased risk for cardiovascular disorders, sustained inflammation, and susceptibility to infections[1][3][5][6].
Ligand internalization: Drugs or antibodies may block binding/uptake of modified LDL or pathogens. Immune modulation: Targeting SR-A1 can reduce inflammatory signaling. Preventing foam cell formation: Inhibitors may block lipid uptake, thus limiting atherosclerosis progression.
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