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Vol. 13, Art. 76 (pp. 900-922)    |    2012       

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MACROPHAGES AND LIPOPROTEIN METABOLISM IN ATHEROSCLEROTIC LESION

Nikiforov Nikita1,2,4, Gratchev Alexei1,2, Sobenin Igor2, Orekhov Alexander2,3, and Julia Kzhyhskowska1,2

1Medical Faculty Mannheim, Ruprecht-Karls University of Heidelberg, Mannheim, Germany (Theodor-Kutzer Ufer 1-3, 68167 Mannheim, Germany, Tel: +49 621 383 2440, Fax: +49 621 383 3815, E-Mail: julia.kzhyshkowska@umm.de); 2Institute of General Pathology and Pathophysiology, Russian Academy of Medical Sciences, Moscow, Russia; 3Institute for Atherosclerosis Research, Skolkovo Innovative Centre; 4Moscow Institute of Physics and Technology (State University).

Brief summary

Atherosclerosis is one of the most life-threatening human disorders leading to myocardial infarction, unstable angina, sudden cardiac death, and ischemic stroke. Currently it is established that atherosclerosis is a chronic inflammatory disorder characterised by the development of lesions in intima of major arteries. Key role in the development of atherosclerosis play pathological cross-talk between plasma lipoproteins and cells of intima, such as monocytes/macrophages, resulting in the development of foamy cells that constitute a major component of atherosclerotic plaque. In our review we focus on the major cellular and molecular processes leading to the formation and accumulation of foamy cells: increased transmigration of monocytes into sub-endothelial sites of inflammation, activation of macrophages, modifications of lipoproteins, different types of uptake of native and associated lipoproteins (endocytosis, phagocytosis, and less-investigated – patocytosis), as well as participation of different molecular systems in the reverse cholesterol transport in macrophages. Special attention is given to the recent data indicating that scavenger receptors participate not only in the uptake of modified lipoproteins, but also in the reverse cholesterol transport. In conclusion, we discuss most relevant open questions in our understanding of the mechanism and functional consequences of macrophage/lipoprotein interactions: which receptor systems are used for the recognition and internalisation of aggregated lipoproteins, what are the mechanisms of intracellular processing of associated lipoproteins, and how associated lipoproteins affect functional programming of macrophages.


Key words

atherosclerosis, lipoprotein, endocytosis, phagocytosis, scavenger receptor, monocyte, macrophage, inflammation.

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