SAA, HDL biogenesis, and inflammation

The understanding of Tangier disease has, over the last decade, focused attention on the role of the ABC transporter ABCA1 in the biogenesis of HDL (1). Both hepatic and extrahepatic ABCA1 expression are important in the regulation of plasma HDL levels (2). The level of HDL is thought to be critical in inhibiting lesion formation as well as in reducing the lipid load of preexisting atherosclerotic lesions. However, it is not only the level of HDL that is relevant for its atheroprotective properties; the quality of the HDL is also important (3).