Atherosclerotic plaque formation

Veillard NR, Kwak B, Pelli G, et al. Antagonism of RANTES receptors reduces atherosclerotic plaque formation in mice. Circ Res 2004 94(2) 253-261. 

E (a-tocopherol) Antioxidant in the hpid phase. Protects membrane lipids from peroxidation and helps prevent oxidation of LDL particles thought to be involved in atherosclerotic plaque formation... 

Raines EW, Ross R. Biology of atherosclerotic plaque formation possible role of growth factors in lesion development and the potential impact of soy. J. Nutr. 125, 624S-630S, 1995. 

Hyperlipidemia can lead to atherosclerosis and subsequent cardiovascular incidents such as thrombosis and infarction. This condition is often treated by a combination of drug therapy and diet and life-style modifications. Pharmacologic interventions are typically targeted toward decreasing the synthesis of harmful (atherogenic) plasma components, including certain lipoproteins (IDL, LDL, VLDL) that are associated with atherosclerotic plaque formation. 

Of the many disorders of lipoprotein metabolism (Tables 5.2 and 5.3), familial hypercholesterolaemia type II may be the most prevalent in the general population. It is an autosomal dominant disorder that results from mutations affecting the structure and function of the ceU-surface receptor that binds plasma LDLs and removes them from the circulation. The defects in LDL-receptor interaction result in lifelong elevation of LDL cholesterol in the blood. The resultant hypercholesterolaemia leads to premature coronary artery disease and atherosclerotic plaque formation. Familial hypercholesterolaemia was the first inherited disorder recognised as being a cause of myocardial infarction (heart attack). 

Due to the fact the PAD is the result of atherosclerotic plaque formation in the arteries that results in decreased blood flow to the legs. 

The mRNA induction of PDGF, bFGF and TGF pi in vascular SMC in vitro and in vivo as a direct consequence of an endothelial lesion or atherosclerotic plaque formation is preceded by the activation of several immediate-early genes [314,315]. In particular, PDGF and TGF pi expression, unlike that of bFGF, is dependent on early protein synthesis [315]. There is compelling evidence that the products of these immediate-early... 

Durak, I. et al.. Effects of garlic extract on oxidant/antioxidant status and atherosclerotic plaque formation in rabbit aorta, Nutr. Metab. Cardiovasc. Dis., 12, 141, 2002. 

Bursill, C.A., Choudhury, R.P., Ali, Z., Greaves, D.R., and Channon, K.M. (2004) Broad-spectrum CC-chemokine blockade by gene transfer inhibits macrophage recruitment and atherosclerotic plaque formation in apolipoprotein E-knockout mice. Circulation, 110, 2460-2466. 

Kammerer, I., R. Ringseis, and K. Eder. 2011a. Feeding a thermally oxidised fat inhibits atherosclerotic plaque formation in the aortic root of LDL receptor-deficient mice. JoumglafNjMrUioT 105 190-9. 

Dansky, H. M., Charlton, S. A., Harper, M. M., and Smith, J. D. (1997). T and B lymphocytes play a minor role in atherosclerotic plaque formation in the apolipoprotein E-deficient mouse. Proc. Natl. Acad Sci. USA 94, 4642—4646. 

Several studies have shown that the extent of coronary artery stenosis due to atherosclerotic plaque formation and expansion into the arterial lumen is not sufficient to explain the incidence of clinical events associated with atherosclerosis [183]. It appears that the generation of clinical events involves plaque mpture, resulting in thrombus formation and arterial occlusion. This mpture is induced by vasomotor disturbances in which oxidized low-density lipoproteins may be involved. Resveratrol is able to regulate vasomotion, which is impaired in atherosclerosis. The key regulators of the vasomotor function are the vasodilator NO and the vasoconstrictor endothelin-1 [167]. A number of in vitro and in vivo studies have shown improved vascular function in response to resveratrol [184, 185]. Resveratrol enhances expression and activity of endothelial nitric oxide synthase [186] and inhibits endothelin-1 secretion and endothelin-1 gene expression in human umbilical vein endothelial cells [187]. Intragastric administration of resveratrol for 12 weeks to hypercholesterolemic rabbits improved the endothelial function, reduced plasma endothelin-1 levels, and induced... 

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