@entity165 , XXXX lowering, and endothelial function.

@entity32 @entity1007 @entity301 @entity26 @entity409 @entity1003 @entity842 @entity731 @entity165
A strong relationship between @entity1007 and @entity731 has been established through epidemiological, experimental, and clinical trial data. Traditional theories on the pathophysiology of this relationship involve the deposition, modification, and cellular uptake of @entity165 , and the release of inflammatory and growth factors resulting in smooth muscle cell proliferation and collagen matrix production. The vasculature has recently been found to be an active and complex organ, with the endothelium playing a controlling role in vascular tone, lipid breakdown, thrombogenesis, @entity32 , and vessel growth. In the presence of risk factors such as @entity1007 , the endothelium promotes vasoconstriction, monocyte and platelet adhesion, thrombogenesis, and growth factor release. A high-fat diet also directly impairs endothelial function and @entity1003 factors. @entity409 is associated with decreased availability of the predominant vasodilator @entity842 , possibly by increased destruction by @entity26 free radicals. This dysfunctional state appears before the earliest anatomic evidence of @entity731 and may represent an important initial step in its development. Several studies have shown improvements in endothelial function with @entity165 lowering in both normal individuals and those with @entity301 . Short-term improvements in endothelial-dependent vasodilation and adhesion molecule expression have also been reported with antioxidant therapy. These observations suggest that @entity731 is at least in part caused by @entity409 that favors cellular proliferation. This new understanding helps to explain the early and substantial reductions in major cardiovascular events associated with @entity165 lowering.
