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Role of Interleukins in Relation to the Renin-Angiotensinsystem in Atherosclerosis

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Part of the book series: Progress in Inflammation Research ((PIR))

Abstract

The morphology of human atherosclerotic plaques ranges from a solid fibrous structure to those with substantial lipid cores, covered by only a thin fibrous cap on its luminal aspect [1-4]. Pathological studies have demonstrated that rupture of these coronary atheromas precipitates the formation of the occluding thrombus that causes an acute coronary syndrome, such as unstable angina or myocardial infarction [4]. Plaque-rupture predominantly occurs on the edges of the plaque’s fibrous cap, the shoulder region, areas frequently associated with accumulations of monocyte-derived macrophages, T lymphocytes and mast cells in close proximity to vascular smooth muscle cells [1,4,5]. These activated macrophages and T lymphocytes stimulate their neighboring cells to erode the collagen and elastin, via the release of inflammatory cytokines, resulting in a decay of the framework which forms the plaque’s cap and ultimately leading to the plaque’s rupture [1,5,6].

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Schieffer, B., Drexler, H. (2001). Role of Interleukins in Relation to the Renin-Angiotensinsystem in Atherosclerosis. In: Mehta, J.L. (eds) Inflammatory and Infectious Basis of Atherosclerosis. Progress in Inflammation Research. Birkhäuser, Basel. https://doi.org/10.1007/978-3-0348-8239-2_9

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  • DOI: https://doi.org/10.1007/978-3-0348-8239-2_9

  • Publisher Name: Birkhäuser, Basel

  • Print ISBN: 978-3-0348-9487-6

  • Online ISBN: 978-3-0348-8239-2

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