Key result
A high-fat diet induces red blood cell dysfunction, which promotes atherosclerosis by enhancing the recruitment of inflammatory monocytes.
Highlights new experimental evidence that red blood cell dysfunction induced by a high-fat diet promotes atherosclerosis via inflammatory monocyte recruitment.
T he initiation, progression, and complications of athero- sclerosis 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 al 3 and Kolodgie et al 4 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 al 5 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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Simon et al. (2015) conducted an editorial in Atherosclerosis. High-fat diet was evaluated on Atherosclerosis progression via RBC dysfunction and inflammatory monocyte recruitment. A high-fat diet induces red blood cell dysfunction, which promotes atherosclerosis by enhancing the recruitment of inflammatory monocytes.
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