The following article in the April 18, 2008 issue of Circulation describes oxLDL's key role in atherosclerosis versus total cholesterol, LDL cholesterol, and triglycerides. The study used apolipoprotein E-deficient knockout mice. When fed a high fat diet their cholesterol increases substantially and, as a consequence, plaque lesions are formed rather rapidly. Next, the research team injected a receptor into the liver to reduce circulating oxLDL, and the lesions stabilized. The findings are summarized below:


Mice with high cholesterol (T-Cholesterol, LDL, Triglycerides) and high oxidized LDL had "markedly increased" atherosclerotic lesions.


Mice with high cholesterol (T-Cholesterol, LDL, Triglycerides) and low oxidized LDL had "complete protection" of atherosclerotic progression.


Reduction of oxidized LDL resulted in “complete prevention of atherosclerotic progression despite the persistence of severe LDL hypercholesterolemia and hypertriglyceridemia.”

OXIDIZED LDL IS THE KEY MOLECULE DIRECTLY INVOLVED IN THE DELOPMENT AND PROGRESSION OF ATHROSCLEROTIC PLAQUE

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National Screening Institute (NSI) has the exclusive world-wide rights to oxidized LDL and malondialdehyde (MDA)-modified LDL antibodies and corresponding technology developed by Professor Paul Holvoet at the University of Leuven, Belgium.