title: Atherosclerosis: humoral and cellular factors of inflammation.
abstract: In the past decade, atherosclerosis has come to be recognized as active and inflammatory rather than simply a passive process of lipid infiltration or a reparative process after endothelial injury. In general, atherosclerosis can be considered as an intramural chronic inflammation resulting from interactions between modified lipoproteins, monocyte-derived macrophages, lymphocytes, and the normal cellular elements of the arterial wall. The process of inflammation occurs in response to functional and structural injury through a variety of known and unknown stimuli and is active over years and decades. Here, we review recent experimental and human studies of inflammatory mechanisms underlying the pathogenesis of atherosclerosis.
authors.affiliation: Department of Diagnostic Radiology, Universitätsklinikum, Klinikstr. 36, 35392, Giessen, Germany.
authors.forename: A C
authors.initials: AC
authors.lastname: Langheinrich
authors.forename: R M
authors.initials: RM
authors.lastname: Bohle
mesh_terms: D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology* / Q000276:immunology / Q000473:pathology; D003952:Diagnostic Imaging; D004195:Disease Models, Animal; D042783:Endothelial Cells; D006710:Homocysteine / Q000097:blood; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D007239:Infections; D007249:Inflammation / Q000150:complications* / Q000473:pathology; D007962:Leukocytes; D051379:Mice; D009569:Nitric Oxide / Q000096:biosynthesis
chemical_list: D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D006710:Homocysteine; D009569:Nitric Oxide