Research conducted at the Cleveland Clinic in Ohio, USA, has characterized a region within the high-density lipoprotein molecule, the most common carrier for "good" cholesterol, that can become dysfunctional and inhibit the body's ability to fight cholesterol build up.
The team, which was led by Stanley Hazen, the clinic's head of preventative cardiology and rehabilitation, identified a key functional domain which, if modified through the action of the enzyme myeloperoxidase present in atherosclerotic plaques, becomes unable to remove cholesterol molecules from the cell wall. Full data from the study are published in the August 5 edition of the journal Nature Structural & Molecular Biology.
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