Resident intimal dendritic cells and the initiation of atherosclerosis.
PURPOSE OF REVIEW: To highlight the fact that regional differences in the normal arterial intima are critical to atherosclerotic lesion formation driven by systemic risk factors. RECENT FINDINGS: At arterial curvatures, bifurcations and branches unique hemodynamics influence endothelial cell signaling and gene expression patterns, which create a proinflammatory environment, with low-grade recruitment of monocytes and accumulation of cells with dendritic features in the intima. Upon induction of hypercholesterolemia, these resident intimal dendritic cells initiate atherosclerosis by rapidly engulfing lipid and becoming the first foam cells in nascent lesions. This step precedes endothelial cell activation and increased monocyte recruitment. SUMMARY: The unique features of the arterial intima at atherosclerosis-susceptible sites do not lead to disease under normal physiological conditions, but this intimal environment promotes the initiation of atherogenesis upon induction of systemic risk factors such as hypercholesterolemia.[1]References
- Resident intimal dendritic cells and the initiation of atherosclerosis. Cybulsky, M.I., Jongstra-Bilen, J. Curr. Opin. Lipidol. (2010) [Pubmed]
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