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The initiation, progression, and complications of atherosclerosis are mediated by a complex interplay of hematopoietic cells, vascular cells, and the extracellular matrix in response to metabolic (eg, hyperlipidemia, diabetes mellitus) and environmental (eg, smoking) injury.1 Recruitment and activation of immune cells of hematopoietic origin are key elements in the development of atherosclerosis.2 Elegant experimental studies, typically performed in compound mutant mice susceptible to diet-induced atherosclerosis, indicate important roles for monocytes, T lymphocytes, neutrophils, and mast cells in lesion formation. Although Barger et al3 and Kolodgie et al4 proposed a role for vasa vasorum, neovascularization, and intraplaque hemorrhage with extravasation of red blood cells (RBCs) as a mechanism of atherosclerotic lesion progression, a direct contribution of RBCs in atherogenesis is uncertain. In this issue of Circulation, Unruh et al5 report that a high-fat diet induces RBC dysfunction, which is capable of promoting atherosclerosis by enhancement of the recruitment of inflammatory monocytes.
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The main physiological function of RBCs is to transport respiratory gases, including O2, CO2, and nitric oxide, throughout tissues. However, a series of studies spanning the past decade demonstrate that RBCs express adhesion molecules and multiple classes of receptors (eg, complement, scavenger, G protein–coupled, and chemokine), thereby raising the possibility that functional interactions of RBCs with leukocytes, platelets, endothelial cells, plasma proteins, and lipoproteins may be important in health and disease (Hermand …