title: PON-dering differences in HDL function in coronary artery disease.
abstract: HDL cholesterol activates endothelial cell production of the atheroprotective signaling molecule NO, and it promotes endothelial repair. In this issue of the JCI, Besler et al. provide new data indicating that HDL from stable coronary artery disease (CAD) or acute coronary syndrome patients inhibits rather than stimulates endothelial NO synthesis and endothelial repair. This may be related to decreased HDL-associated paraoxonase 1 (PON1) activity. These observations support the concept that the cardiovascular impact of HDL is not simply related to its abundance, and the translation of the present findings to prospective studies of CAD risk and to evaluations of HDL-targeted therapeutics is a logical future goal.
authors.affiliation: Division of Pulmonary and Vascular Biology, Department of Pediatrics, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9063, USA.
authors.forename: Chieko
authors.initials: C
authors.lastname: Mineo
authors.forename: Philip W
authors.initials: PW
authors.lastname: Shaul
mesh_terms: D000818:Animals; D003324:Coronary Artery Disease / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000378:metabolism*; D005260:Female; D006801:Humans; D008075:Lipoproteins, HDL / Q000378:metabolism*; D008297:Male; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism*
chemical_list: D008075:Lipoproteins, HDL; C496314:NOS3 protein, human; D052250:Nitric Oxide Synthase Type III