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 Macrophages

General considerations

  • Macrophage production.
  • Macrophage kinetics.
  • Macrophage function.

The role of macrophages in vascular disease

  • Chemoattractants.
  • Monocyte endothelial cell adherence.
  • Monocyte migration.
  • Macrophage activation.

Macrophage secretory products

  • Proteases and local tissue destruction.
  • Cytokines (including interleukin-1, interleukin-6, interleukin-8, interferon, tumor necrosis factor and colony stimulating factors).
  • Growth factors (including platelet-derived growth factor, fibroblast growth factor and transforming growth factor- β ).

The role of macrophages in lipid metabolism

References

Plenz G, Robenek H. Monocytes/macrophages in atherosclerosis. Eur Cytokine Netw 1998;9:701-703.

In this chapter the role of the monocyte/macrophage in the genesis of the atherosclerotic plaque is discussed. As it is demonstrated, the pivotal role of the macrophage in atherosclerosis depends not only on its ability to handle lipids but also on its physical and secretory functions and its role as a mediator of inflammation.

Yla-Herttuala S. Macrophages and oxidized low density lipoproteins in the pathogenesis of atherosclerosis. Ann Med 1991;23:561-567.

This article describes the role of macrophages and oxidized low density lipoproteins in the pathogenesis of atherosclerosis. The clarification of this role offers an interesting possibility to reduce atherosclerosis by antioxidants, enzyme inhibitors and other compounds that protect LDL against oxidative damage and/or reduce the subsequent harmful effects of oxidized LDL on various cellular functions.

Rosenfeld ME, Palinski W, Yla-Herttuala S, Carew TE. Macrophages, endothelial cells, and lipoprotein oxidation in the pathogenesis of atherosclerosis. Toxicol Pathol 1990;18:560-571.

This review outlines the complex interactions between macrophages, endothelial cells, and lipoprotein oxidation in the pathogenesis of atherosclerosis. The basic steps of the pathogenetic pathway including trapping of LDL, oxidation of LDL, monocyte chemotaxis, cell transformation into macrophage-derived foam cells, endothelial cell injury and formation of mural thrombi are summarized.

Aviram M, Fuhrman B. LDL oxidation by arterial wall macrophages depends on the oxidative status in the lipoprotein and in the cells: role of prooxidants vs. antioxidants. Mol Cell Biochem 1998;188:149-159.

All major cells in the arterial wall including endothelial cells, smooth muscle cells and monocyte derived macrophages can oxidize LDL. Oxidized LDL is highly atherogenic as it stimulates macrophage cholesterol accumulation and foam cell formation, it is cytotoxic to cells of the arterial wall and it stimulates inflammatory and thrombotic processes. This review article summarizes the above issues with an emphasis on the authors' own data.

DiCorleto PE . Cellular mechanisms of atherogenesis. Am J Hypertens 1993;6:314S-318S.

The interactions of endothelial cells, smooth muscle cells, and monocyte-derived macrophages as well as the role of thrombin, monocyte adhesion proteins and platelet-derived growth factor in atherogenesis has been the focus of great interest over the past decades. The resultant information is summarized in this brief review.

Posted June 2010