title: The pathogenesis of atherosclerosis.
abstract: Worldwide, more people die of the complications of atherosclerosis than of any other cause. It is not surprising, therefore, that enormous resources have been devoted to studying the pathogenesis of this condition. This article attempts to summarize present knowledge on the events that take place within the arterial wall during atherogenesis. Classical risk factors are not dealt with as they are the subjects of other parts of this book. First, we deal with the role of endothelial dysfunction and infection in initiating the atherosclerotic lesion. Then we describe the development of the lesion itself, with particular emphasis on the cell types involved and the interactions between them. The next section of the chapter deals with the events leading to thrombotic occlusion of the atherosclerotic vessel, the cause of heart attack and stroke. Finally, we describe the advantages--and limitations--of current animal models as they contribute to our understanding of atherosclerosis and its complications.
authors.affiliation: Institute of Arteriosclerosis Research, Münster, Germany. cullen@uni-muenster.de
authors.forename: P
authors.initials: P
authors.lastname: Cullen
authors.forename: J
authors.initials: J
authors.lastname: Rauterberg
authors.forename: S
authors.initials: S
authors.lastname: Lorkowski
mesh_terms: D000818:Animals; D017209:Apoptosis; D050197:Atherosclerosis / Q000209:etiology*; D002784:Cholesterol / Q000378:metabolism; D004195:Disease Models, Animal; D004730:Endothelium, Vascular / Q000502:physiology; D005109:Extracellular Matrix / Q000502:physiology; D005487:Foam Cells / Q000502:physiology; D006801:Humans; D007239:Infections / Q000150:complications; D008264:Macrophages / Q000502:physiology; D008407:Mast Cells / Q000502:physiology; D009000:Monocytes / Q000502:physiology; D009336:Necrosis
chemical_list: D002784:Cholesterol