Atherosclerosis decreasing

Peripheral vascular disease, often one of the sequelia of atherosclerosis, is characterized by markedly decreased circula-... 

Current evidence suggests that PPAR activation may limit inflammation and hence atherosclerosis. Both PPAR-a and PPAR-y can reduce T-cell activation, as shown by decreased production of EFN-y. PPAR-a agonists also rqness endothelial VCAM-1 expression and inhibit the inflammatory activation of vascular SMCs, while PPAR-y agonists repress endothelial chemokine expression and decrease macrophage MMP production. 

Atherosclerosis is a disease characterized by deposits of fatty plaques on the inner wall of arteries. These deposits result in a narrowing of the lumen (inside diameter) of die artery and a decrease in blood supply to the area served by die artery. 

An increase in serum lipids is believed to contribute to or cause atherosclerosis, a disease characterized by deposits of fatty plaques on the inner walls of arteries. These deposits result in a narrowing of the lumen (inside diameter) of the artery and a decrease in blood supply to the area served by the artery. When these fatty deposits occur in the coronary arteries, the patient experiences coronary artery disease. Lowering blood cholesterol levels can arrest or reverse atherosclerosis in the vessels and can significantly decrease the incidence of heart disease. 

Cardiovascular disease (CVD) is one of the leading causes of death worldwide. There are a number of established risk factors including serum cholesterol levels, smoking and family history, which are responsible for between 50 and 75% of the CVD cases, with the remainder due to factors that cause atherosclerosis. Estrogen treatment such as hormone replacement therapy is known to protect against CVD by decreasing the levels of low-density... 

The successful outcome in cholesterol management is to reduce cholesterol and triglycerides below the NCEP ATP III goals in an effort to alter the natural course of atherosclerosis and decrease future cardiovascular events. 

Boring L, Gosling J, Cleary M, Charo IF. Decreased lesion formation in CCR2 / mice reveals a role for chemokines in the initiation of atherosclerosis. Nature 1998 394 894-7. 

Growing clinical data also points to the importance of IL-8 in atherogenesis. IL-8 has been found in atheromatous lesions from patients with atherosclerotic disease including carotid artery stenosis (103), CAD (118), abdominal aortic aneurysms (AAA) (103,104,114), and peripheral vascular disease (PVD) (104). Furthermore, studies using plaque explant samples have yielded more direct evidence for IL-8 involvement. Media from cultured AAA tissue induced IL-8-dependent human aortic endothelial cell (HAEC) chemotaxis (122). Homocysteine, implicated as a possible biomarker for CAD, is also capable of inducing IL-8 (123-125) by direct stimulation of endothelial cells (123,124) and monocytes (125). When patients with hyperhomocysteinemia were treated with low-dose folic acid, decreases in homocysteine levels correlated with decreases in IL-8 levels (126). Statins significantly decrease serum levels of IL-6, IL-8, and MCP-1, as well as expression of IL-6, IL-8, and MCP-1 mRNA by peripheral blood monocytes and HUVECs (127). Thus, IL-8 may be an underappreciated factor in the pathogenesis of atherosclerosis. 

Lesnik P, Haskell CA, Charo IF. Decreased atherosclerosis in CX3CRI mice reveals a role for fractalkine in atherogenesis. J Clin Invest 2003 111(3) 333—340. 

CCR2 deficiency results in decreased atherosclerosis in vessels of susceptible mice. 2. Decreased intimal hyperplasia in femoral artery injury model of atherosclerosis seen with CCR2 deficiency. CCR2 expression is increased in the monocytes of hypercholesterolemic patients. 

Napoli et al. [286] found that the nifedipine treatment of stroke-prone spontaneously hypertensive rats (SPSHR) suppressed the plasma and LDL oxidation and the formation of oxidation-specific epitopes and increased the survival of rats independently of blood pressure modification. Their results suggest that the protective effects of calcium blockers of dihydro-pyridine-type on cerebral ischemia and stroke may, at least in part, depend on their antioxidant activity. In vivo antioxidant effect of nilvadipine on LDL oxidation has been studied in hypertensive patients with high risk of atherosclerosis [287], It was found that there was a significant decrease in the level of LDL cholesterol oxidation in patients after nilvadipine treatment. 

The disturbance of balance between superoxide and nitric oxide occurs in a variety of common disease states. For example, altered endothelium-dependent vascular relaxation due to a decrease in NO formation has been shown in animal models of hypertension, diabetes, cigarette smoking, and heart failure [21]. Miller et al. [22] suggested that a chronic animal model atherosclerosis closely resembles the severity of atherosclerosis in patients. On the whole, the results obtained in humans, for example, in hypertensive patients [23] correspond well to animal experiments. It is important that endothelium-dependent vascular relaxation in patients may be improved by ascorbic acid probably through the reaction with superoxide. 

Fig. 9.5. Protection by SERMs against atherosclerosis has been researched in animals. In a model of ovariectomized rabbits, raloxifene reduced the cholesterol content in the inner part of the aorta more than placebo did (upper panel). This effect was more intense in animals treated with estradiol (Bjarnason et al. 1997). In contrast, in a different model of oophorectomized monkeys (lower panel), estradiol, and not raloxifene at two different dosages, significantly decreased the size of atherosclerotic plaques (Clarkson et al. 1998)...

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