High-normal phosphate levels linked to early atherosclerosis
Healthy adults with higher levels of phosphate in the blood are more likely to have
increased levels of calcium in the coronary arteries—a key indicator of
atherosclerosis and future cardiovascular disease risk, reports a study in the February
2009 issue of the Journal of the American Society of Nephrology (JASN). "Phosphate
level may represent a previously unidentified and modifiable cardiovascular risk factor,
and could help identify people for whom modifiable risk factors could be screened and
managed," comments Robert N. Foley, MD, of University of Minnesota and the US Renal
Data System (USRDS), both in Minneapolis, MN. Dr. Foley and colleagues studied the
relationship between phosphate levels and coronary artery calcium in 3,015 healthy young
adults from a long-term study of risk factors for coronary artery disease. At an average
age of 25 years, the subjects underwent measurement of their serum phosphate level. The
phosphate level reflects the mineral phosphorus, which plays an important role in bone
metabolism.A special computed tomography (CT) scan was used 15 years later to measure the
level of calcium in the coronary arteries. Coronary artery calcium is an early sign of
atherosclerosis, or "hardening of the arteries."
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Aspirin and atherosclerosis
Aspirin has become one of the most widely used medications in the world, owing to its
ability to reduce pain, fevers, inflammation, and blood clotting. In animal studies,
aspirin has also been shown to prevent atherosclerosis, though none of its known
mechanisms of action would seem to account for this. In a new study, though, researchers
have uncovered the mechanism that may explain aspirin's ability to prevent arterial plaque
buildup. Using cell culture and mouse models, Sampath Parthasarathy and colleagues
observed that aspirin –specifically its active byproduct salicylate– can greatly
increase the expression of two proteins: paraoxonase 1 (PON1) and apolipoprotein A1
(ApoA1); in the mouse studies, low dose aspirin supplements could increase PON1 and ApoA1
levels by 7- and 12- fold, respectively. Both of these proteins are beneficial components
of the HDL complex, the "good cholesterol" that helps prevent atherosclerosis;
ApoA1 removes bad cholesterol from the bloodstream while PON1 is an antioxidant that
breaks down toxic lipid peroxides. The researchers also noted that the heightened
expression of PON1 was accompanied by an increase in a receptor called AHR (aryl
hydrocarbon receptor); this was intriguing as a chemical known to attach to AHR is
resveratrol, the "heart healthy" component of red wine.
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Genes that protect against
atherosclerosis identified
One way of combating atherosclerosis is to reduce levels of "bad cholesterol" in
the blood. Scientists at the Swedish medical university Karolinska Institutet have now
identified the genes that bring about this beneficial effect.
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Friend or foe? How the body's
clot-busting system speeds up atherosclerosis
Sometimes it's hard to tell friends from foes, biologically speaking. Naturally produced
in the body, urokinase plasminogen activator and plasminogen interact to break up blood
clots and recruit clean-up cells to clear away debris related to inflammation. In fact,
urokinase manufactured as a drug effectively clears clogged arteries by generating
clot-busting plasmin from blood-derived plasminogen. However, despite the efficacy of
urokinase and plasmin in clearing blood clots, evidence has shown that humans with a high
baseline level of blood plasmin are at increased risk for heart attacks and for
fast-developing forms of atherosclerosis. In addition, human arteries affected by
atherosclerosis have an abundance of urokinase. These associations between plasmin,
urokinase and increased atherosclerosis counter the notion that urokinase and plasmin
protect against heart attacks by removing dangerous blood clots. At first vascular
biologists didn't know how to interpret these findings. Specifically, they wondered
whether the high level of urokinase in atherosclerotic artery walls was contributing to
atherosclerosis or was evidence of the body's efforts to fight it. To try to resolve this
puzzle, Dr. David A. Dichek, the John Locke Jr. Family Endowed Professor of Cardiology and
associate director for research in the Division of Cardiology at the University of
Washington (UW), and his team generated mice that were genetically engineered to produce
more urokinase in their artery walls. These mice developed arteries with worse
atherosclerosis, including thicker walls, narrower interiors, and limited blood flow. The
mice died suddenly with clogged arteries and evidence of heart attacks. Dichek noted other
reasons why his team expected that increased activity of the urokinase/plasminogen system
would promote atherosclerosis, including the roles of urokinase and plasminogen in
inflammation and cell migration.
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