The Pathogenesis of Atherosclerosis: Atherogenesis and Inflammation View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

1989

AUTHORS

J. Michael Munro , Ramzi S. Cotran

ABSTRACT

Atherosclerosis and its complications, such as myocardial infarction, stroke, and peripheral vascular disease, remain major causes of morbidity and mortality in the Western World; coronary heart disease alone accounts for over half a million deaths in the United States annually (4). Because atherosclerosis is a slowly progressive disease, which begins in childhood and does not become manifest until middle-age or later, its etiology and pathogenesis have been difficult to elucidate. Yet in the past decade or two, cellular and molecular approaches to the study of the cells of the vascular wall, as well as innovative methods for examination of abnormalities in lipid metabolism, have provided numerous insights into the pathogenesis of atherosclerosis. One of these insights is the resurgent appreciation that atherosclerosis is a response of the vascular wall to injury (117–119), having many of the features of the inflammatory response in other tissues (81, 119). Atherosclerosis was likened to inflammation by Rayer in 1823 (112), and this concept was extended by Virchow (145) a few decades later; in 1950, Saphir and Gore (124) spoke of the evidence for an inflammatory basis of coronary arteriosclerosis in the young, and most recently Joris and Majno (81) stressed the similarities between the two processes. That atherosclerosis has similarities to inflammation will be apparent from the considerations which follow, as will be the implications of these concepts to future work on the pathogenesis of atherosclerosis and its prevention and treatment. More... »

PAGES

171-183

Book

TITLE

Pathology Reviews · 1989

ISBN

978-1-4612-8849-7
978-1-4612-4502-5

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-1-4612-4502-5_10

DOI

http://dx.doi.org/10.1007/978-1-4612-4502-5_10

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1045274210


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150 schema:description Atherosclerosis and its complications, such as myocardial infarction, stroke, and peripheral vascular disease, remain major causes of morbidity and mortality in the Western World; coronary heart disease alone accounts for over half a million deaths in the United States annually (4). Because atherosclerosis is a slowly progressive disease, which begins in childhood and does not become manifest until middle-age or later, its etiology and pathogenesis have been difficult to elucidate. Yet in the past decade or two, cellular and molecular approaches to the study of the cells of the vascular wall, as well as innovative methods for examination of abnormalities in lipid metabolism, have provided numerous insights into the pathogenesis of atherosclerosis. One of these insights is the resurgent appreciation that atherosclerosis is a response of the vascular wall to injury (117–119), having many of the features of the inflammatory response in other tissues (81, 119). Atherosclerosis was likened to inflammation by Rayer in 1823 (112), and this concept was extended by Virchow (145) a few decades later; in 1950, Saphir and Gore (124) spoke of the evidence for an inflammatory basis of coronary arteriosclerosis in the young, and most recently Joris and Majno (81) stressed the similarities between the two processes. That atherosclerosis has similarities to inflammation will be apparent from the considerations which follow, as will be the implications of these concepts to future work on the pathogenesis of atherosclerosis and its prevention and treatment.
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