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Size-dependent effects of particles around 0.5–1 μm disrupt the p38 MAPK/Smad2/Src/ERK/PLCγ1 pathways, inducing autophagy and endothelial necrosis [81], and the surface chemistry of the particles determines their effect on hemostasis [37,38]: aminated surfaces activate platelets through receptor-dependent mechanisms [86], and carboxylated ones through the intrinsic pathway, with a dose-dependent correlation observed between particle count and degree of platelet activation [87]

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