The Yin and Yang of Oxidation in the Development of the Fatty Streak: A Review Based on the 1994 George Lyman Duff Memorial Lecture

• Published in: Arteriosclerosis, thrombosis, and vascular biology Vol. 16; no. 7; pp. 831 - 842
• Main Authors: Navab, Mohamad, Berliner, Judith A, Watson, Andrew D, Hama, Susan Y, Territo, Mary C, Lusis, Aldons J, Shih, Diana M, Van Lenten, Brian J, Frank, Joy S, Demer, Linda L, Edwards, Peter A, Fogelman, Alan M
• Format: Journal Article
• Language: English
• Published: Philadelphia, PA American Heart Association, Inc 01.07.1996; Hagerstown, MD Lippincott
• Subjects: Animals; Arteries - metabolism; Arteriosclerosis - etiology; Arteriosclerosis - genetics; Atherosclerosis (general aspects, experimental research); Biological and medical sciences; Blood and lymphatic vessels; Cardiology. Vascular system; Humans; Lipid Peroxidation; Lipoproteins, HDL - metabolism; Lipoproteins, LDL - metabolism; Medical sciences; Phospholipids - metabolism; Human; Genetic inheritance; Pathophysiology; Pathogenesis; Cardiovascular disease; Inflammation; Metabolism; Fatty acids; Vascular disease; Lipoprotein LDL; Regulation(control); Atherosclerosis; Oxidation
• ISSN: 1079-5642; 1524-4636
• DOI: 10.1161/01.ATV.16.7.831

Recent data support the hypothesis that the fatty streak develops in response to specific phospholipids contained in LDL that become trapped in the artery wall and become oxidized as a result of exposure to the oxidative waste of the artery wall cells. The antioxidants present within both LDL and the microenvironments in which LDL is trapped function to prevent the formation of these biologically active, oxidized lipids. Enzymes associated with LDL and HDL (eg, platelet activating factor acetylhydrolase) or with HDL alone (eg, paraoxonase) destroy these biologically active lipids. The regulation and expression of these enzymes are determined genetically and are also significantly modified by environmental influences, including the acute-phase response or an atherogenic diet. The balance of these multiple factors leads to an induction or suppression of the inflammatory response in the artery wall and determines the clinical course. (Arterioscler Thromb Vasc Biol. 1996;16:831-842.)