This article originally posted 22 March, 2005 and appeared in Issue 252
New Link Between C-Reactive Protein, and Heart Disease and Stroke
The cells that line the arteries are able to produce C-reactive protein, according to a study.
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The cells that line the arteries are able to produce C-reactive protein. C-reactive
protein is a risk marker for heart disease and is known to be produced in the
liver, but UC Davis School of Medicine researchers Ishwarlal Jialal and Sridevi
Devaraj found that endothelial cells also produce C-reactive protein, a key finding
that helps to explain how plaque formation is initiated. This is particularly
important because endothelial cells are supposed to protect the arteries from
C-reactive protein.
“This is an extremely important finding,” says Jialal, professor of
pathology and internal medicine and director of the Laboratory for Atherosclerosis
and Metabolic Research at UC Davis Medical Center. “We have convincingly
demonstrated in this paper that aortic and coronary artery endothelial cells produce
and secrete C-reactive protein. We also showed within the artery, mature white
cells, called macrophages, make chemical messengers, cytokines, which enhance
the C-reactive protein secretion by endothelial cells at least 10-fold.
“This tells us that there is cross-talk in the active plaque where these
cells act in concert to cause very high C-reactive protein levels in the atheroma,
which is the accumulation of plaque on the innermost layer of the artery,”
Jialal said. “The C-reactive protein produced by endothelial cells can not
only act on the endothelial cells, but also on macrophages and smooth muscle cells
in the atheroma. This creates a vicious cycle, leading to plaque instability and
rupture, and ultimately heart attacks and strokes.”
Work at UC Davis and other institutions has shown that C-reactive protein induces
endothelial cell dysfunction, thus promoting plaque formation. C-reactive protein
causes endothelial cells to produce less nitric oxide and to increase the number
of cell adhesion molecules. This, in turn, allows damaging leukocytes to enter
the vessels. Devaraj and Jialal also showed that C-reactive protein induces endothelial
cells to produce plasminogen activator inhibitor, or PAI-1, which promotes clot
formation. In addition, recent studies suggest that plaque tissue also produces
C-reactive protein.
Coronary heart disease is the nation’s single leading cause of death. According
to the American Heart Association, approximately 1.2 million Americans will have
a coronary attack this year. Almost a half million of these people will die. About
7.1 million Americans have survived a heart attack. And another 6.4 million Americans
have experienced chest pain or discomfort due to reduced blood supply to the heart.
The good news is that reducing the concentration of C-reactive protein with targeted
drugs, such as statins, has been shown to reduce cardiovascular events. Treating
other risk factors such as smoking, obesity, high blood pressure and high cholesterol
are also shown to reduce the levels of C-reactive protein.
American Journal of Pathology, April 2005.
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DID YOU KNOW:
Crestor Improves C-Reactive Protein in U.S. Blacks: 10 mg of Crestor lowered CRP
by 14%. An unusual study focusing on black Americans shows that AstraZeneca Plc's
Crestor lowers levels of C-reactive protein, which may be predictive of serious
cardiovascular disease. Presented at the meeting of the American College of Cardiology
in Orlando, Florida, last week focuses on a lesser-known predictor of heart disease
risk -- CRP.
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