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Editorial
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Volume 354:1310-1312 March 23, 2006 Number 12
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Protease Variants, LDL, and Coronary Heart Disease
Alan R. Tall, M.B., B.S.

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 by Cohen, J. C.
-PubMed Citation
Just when we thought we understood everything about low-density lipoprotein (LDL) cholesterol and its relationship to cardiovascular risk, along comes a discovery that reveals a new control mechanism and suggests a strategy for the prevention of atherosclerotic cardiovascular disease.

Plasma levels of LDL cholesterol are in large part determined by the activity of LDL receptors in the liver. Autosomal dominant familial hypercholesterolemia — with its high levels of LDL cholesterol, xanthomas, and premature atherosclerosis — is caused by mutations either in the gene encoding the LDL receptor or in the gene encoding apolipoprotein B — the protein in LDL cholesterol . . . [Full Text of this Article]


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Dr. Tall is a professor of medicine and physiology and the director of the Specialized Center of Research in Molecular Medicine and Atherosclerosis at the Columbia University Medical Center, New York.


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