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Atherosclerosis

Nature volume 407, pages 233–241 (2000)Cite this article

Abstract

Atherosclerosis, a disease of the large arteries, is the primary cause of heart disease and stroke. In westernized societies, it is the underlying cause of about 50% of all deaths. Epidemiological studies have revealed several important environmental and genetic risk factors associated with atherosclerosis. Progress in defining the cellular and molecular interactions involved, however, has been hindered by the disease's aetiological complexity. Over the past decade, the availability of new investigative tools, including genetically modified mouse models of disease, has resulted in a clearer understanding of the molecular mechanisms that connect altered cholesterol metabolism and other risk factors to the development of atherosclerotic plaque. It is now clear that atherosclerosis is not simply an inevitable degenerative consequence of ageing, but rather a chronic inflammatory condition that can be converted into an acute clinical event by plaque rupture and thrombosis.

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Figure 1: Structure of a normal large artery.
Figure 2: Stages in the development of atherosclerotic plaques.
Figure 3: Lesion initiation.
Figure 4: Inflammation.
Figure 5: Foam-cell formation.
Figure 6: Formation of fibrous plaques.
Figure 7: Complex lesions and thrombosis.

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Acknowledgements

I thank R. Chen and K. Wong for help with the preparation of this manuscript and L. Olson for help with the illustrations. Work in my laboratory was supported by NIH grants.

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  1. Department of Medicine, Department of Microbiology Immunology and Molecular Genetics, Department of Human Genetics, and Molecular Biology Institute, University of California, Los Angeles, 90095, California, USA

    Aldons J. Lusis

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Lusis, A. Atherosclerosis. Nature 407, 233–241 (2000). https://doi.org/10.1038/35025203

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