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Atherosclerosis and endothelial damage: A brief overview

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Summary

Atherosclerosis has a complex etiology. Several different cell types are involved, including monocytes, smooth muscle, and endothelial cells. While proliferation of the smooth muscle cells plays a significant role in the development of the “adult” lesion, the initiating step probably involves damage to the endothelial cells of the arterial wall. Injury to these cells may be triggered by a variety of conditions, including hypercholesterolemia, hypertension, cigarette smoking, immune injury, and diabetes. Expression of endothelial injury is complex and involves increased membrane permeability, enhanced monocyte adhesion and infiltration, and an augmented release of growth factors.

The contribution of atherosclerosis to impaired arterial perfusion involves at least two factors: occlusion due to the lesion (rupture, physical obstruction, or accumulated thrombi), and failure of the endothelium-dependent relaxation mechanism. In experimental models of atherosclerosis and in atherosclerosis in humans, calcium antagonists slow the progression of the lesions by a mechanism that is independent of any accompanying vasodilation. These same antagonists also restore the endothelium-dependent relaxation of the vasculature.

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Supported by grants from National Health and Medical Research Council of Australia.

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Nayler, W.G. Atherosclerosis and endothelial damage: A brief overview. Cardiovasc Drug Ther 9 (Suppl 1), 25–30 (1995). https://doi.org/10.1007/BF00878570

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  • DOI: https://doi.org/10.1007/BF00878570

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