Recent studies identify the presence of high-density lipoprotein (HDL) particles in patients
with cardiovascular disease, which are “dysfunctional,” lacking in typical atheroprotective
properties, and promoting proinflammatory effects. The mechanisms for generating
dysfunctional HDL have been unclear. New evidence points to a role for myeloperoxidase
(MPO)-generated oxidants as participants in rendering HDL dysfunctional within human
atherosclerotic plaque. Myeloperoxidase was recently shown to bind to HDL within human …