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Schematic depicts the mechanisms by which our data showed free Hb-induced NF-κB activity, HIF activity, and increased permeability in HMECs-1 through an MyD88-dependent mechanism or reactive oxygen species (ROS) produced from Hb transition states. Hemoglobin-induced MyD88 activation may occur through either a membrane-bound Toll-like receptor (TLR) or through a pattern recognition receptor (PRR) within the endothelial cell.
