Role of Interleukins in Relation to the Renin-Angiotensinsystem in Atherosclerosis View Full Text


Ontology type: schema:Chapter     


Chapter Info

DATE

2001

AUTHORS

Bernhard Schieffer , Helmut Drexler

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]. More... »

PAGES

129-140

Book

TITLE

Inflammatory and Infectious Basis of Atherosclerosis

ISBN

978-3-0348-9487-6
978-3-0348-8239-2

Identifiers

URI

http://scigraph.springernature.com/pub.10.1007/978-3-0348-8239-2_9

DOI

http://dx.doi.org/10.1007/978-3-0348-8239-2_9

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1046869695


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