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Endothelial-Leukocyte Adhesion Molecules in Acute Inflammation and Atherogenesis

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Endothelial Cell Dysfunctions

Abstract

Inflammation and atherosclerosis are pathophysiologic processes which share a common feature in their pathogenesis, the emigration of leukocytes from blood; yet, these processes involve different leukocytes, and have distinct locations, chronologies, and consequences. Acute inflammation is a rapid response of the host to local perturbations, such as trauma or bacterial infection, and is typically followed by resolution.1 A prominent feature of acute inflammation is the emigration of neutrophil leukocytes from the blood of postcapillary venules and small veins into the extravascular space. Atherosclerosis, on the other hand, is a chronic process occurring in arteries, and initially involves the adherence and transmigration of circulating monocytes into the arterial intima.2,3 The result is formation of atherosclerotic lesions that ultimately impinge on the arterial lumen and predispose to complications, such as thrombosis, hemorrhage, embolism, or dissection, which can have serious consequences for tissue perfusion.

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Cybulsky, M.I., Gimbrone, M.A. (1992). Endothelial-Leukocyte Adhesion Molecules in Acute Inflammation and Atherogenesis. In: Simionescu, N., Simionescu, M. (eds) Endothelial Cell Dysfunctions. Springer, Boston, MA. https://doi.org/10.1007/978-1-4899-0721-9_7

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  • DOI: https://doi.org/10.1007/978-1-4899-0721-9_7

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