By Arnold Eckardstein
This e-book supplies an summary on vital mechanisms excited about atherosclerosis and thereby offers pursuits a few of that are used and others that may be worthy for remedy and prevention of atherosclerosis. because atherosclerosis is a multifactorial affliction the scientifc method has to be multidisciplinary. consequently, the authors of this e-book signify diverse components of method starting from uncomplicated, scientific and inhabitants study in addition to diversified fields of workmanship starting from metabolism to immunology and irritation biology and to vascular biology.
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Additional info for Atherosclerosis: Diet and Drugs
C Intimal thickening with xanthoma Stenosis of atherosclerotic vessels is the most common therapeutic target. However, this is the change that is least understood from a histological point of view. In an important paper published in 1987, Seymour Glagov and colleagues reported that human coronary arteries affected by atherosclerosis undergo compensatory enlargement, so that plaque mass does not correlate with the size of the lumen (Glagov et al. 1987; Virmani et al. 2000). Thus, the origin of stenosis of the lumen of atherosclerotic coronary arteries in humans is unknown, though it may be related to an attempt by the artery to heal the atherosclerotic lesion.
Dysfunction of integral membrane proteins Disruption of signalling events Caspase-mediated death Organelle disruption Oxidative damage? Change in balance of survival proteins to death proteins? tional freedom to function properly (Yeagle 1991), such as the Na+ /K+ ATPase, adenylate cyclase, alkaline phosphatase, rhodopsin, and transporters for glucose, organic anions, and thymidine (Tabas 2002). Thus, high free cholesterol levels may in part kill cells by inhibiting one or more vital integral membrane proteins (Table 2).
At some highstress sites such as arterial bifurcations, these processes start as early as The Pathogenesis of Atherosclerosis 33 the ﬁrst weeks of life and even before birth (Velican and Velican 1980). Thus, in infants, enhanced expression of type I and III collagen was localized to smooth muscle cells at a site of pressure-induced intimal thickening on the proximal site of inborn coarctation of the aorta (Jaeger et al. 1990). The formation of a neointima by recruitment of smooth muscle cells from the media is of clinical relevance in the process of restenosis after lumen widening by coronary angioplasty or atherectomy.
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