Although numerous studies have demonstrated anti-atherosclerotic effects of high-density lipoprotein (HDL), drugs that elevate HDL cholesterol levels have failed in the clinic. Stanley Hazen and colleagues provide a potential explanation for this paradox by showing that within human atherosclerotic plaques and plasma of individuals with coronary artery disease, apoA1—the major apolipoprotein present in HDL—is modified by oxidation of a specific tryptophan residue, impairing the anti-atherosclerotic function of apoA1 and HDL.
- Ying Huang
- Joseph A DiDonato
- Stanley L Hazen
