Atherogenic lipoproteins and coronary artery disease: concepts derived from recent advances in cellular and molecular biology.

RW Mahley - Circulation, 1985 - Am Heart Assoc
Circulation, 1985Am Heart Assoc
RECENT ADVANCES have contributed to our understanding of lipoproteins, their
metabolism, and their involvement in atherogenesis (for review see refs. 1 to 6). In this
review, attention will be focusedon specific types of lipoproteins and the mechanisms
whereby they may be either atherogenicor antiatherogenic. Hu-man geneticdiseases of lipid
metabolism and dietinduced changes in lipoproteins have provided unique insights.
Atherosclerotic lesions, as they occur in man or as induced by high-fat, high-cholesterol …
RECENT ADVANCES have contributed to our understanding of lipoproteins, their metabolism, and their involvement in atherogenesis (for review see refs. 1 to 6). In this review, attention will be focusedon specific types of lipoproteins and the mechanisms whereby they may be either atherogenicor antiatherogenic. Hu-man geneticdiseases of lipid metabolism and dietinduced changes in lipoproteins have provided unique insights.
Atherosclerotic lesions, as they occur in man or as induced by high-fat, high-cholesterol diets in experimental animals, share many common properties. Nar-rowing of the vessel lumen is characterized by the deposition of cholesterolin and around cells of the arterial wall in association with cellular proliferation and fibrosis. The cholesterol that accumulates in the arterial wall is derived from plasmalipoproteins; there-fore, to understand the mechanisms involved in athero-genesis, it is important to identify the specific lipopro-teins responsible for the delivery of cholesterol to the cells and to identify the cell type responsible for the accumulation of the cholesterol. Lipid transport into and out of the vessel wall appears to be a constant and dynamic process. Disease of clinical significance de-velops when influxand deposition of cholesterol ex-ceeds egress of cholesterol from the arterial wall. The hyperlipidemia that develops in the genetic diseases to be discussed, or that develops with the consumption of high levels of fatand cholesterol, accelerates the lipid deposition andupsets the balance between influx and egress.
Am Heart Assoc