M
Michael Aviram
Researcher at Technion – Israel Institute of Technology
Publications - 489
Citations - 32705
Michael Aviram is an academic researcher from Technion – Israel Institute of Technology. The author has contributed to research in topics: Cholesterol & Lipoprotein. The author has an hindex of 94, co-authored 479 publications receiving 31141 citations. Previous affiliations of Michael Aviram include University of Tromsø & Steward Health Care System.
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Journal ArticleDOI
Flavonoids-rich nutrients with potent antioxidant activity prevent atherosclerosis development: the licorice example
TL;DR: Glabridin accumulation in macrophages affects cell-signaling processes, which are associated with activation of the cellular NADPH oxidase system, and these phenomena are responsible for the inhibition of cell-mediated oxidation of LDL and the attenuation of atherosclerosis developments by dietary glabridIn.
Book ChapterDOI
Effect of Lipoproteins and Platelets on Macrophage Cholesterol Metabolism
TL;DR: Atherosclerosis is a complicated process that starts with cholesterol accumulation in the cells of the arterial wall, mainly in monocyte-derived macrophages, and later events include the involvement of endothelial cells, smooth muscle cells, platelets, and plasma lipoproteins.
Journal ArticleDOI
Characterization of the PON1 active site using modeling simulation, in relation to PON1 lactonase activity.
TL;DR: The Pon1 possible active site is characterized and a tool which may make it possible to envisage the structure of potential endogenous and exogenous lactones such as the PON1 ligand is proposed.
Journal ArticleDOI
Paraoxonase 2 (PON2) decreases high glucose-induced macrophage triglycerides (TG) accumulation, via inhibition of NADPH-oxidase and DGAT1 activity: studies in PON2-deficient mice.
TL;DR: It is concluded that PON2 has a significant protective role againstmacrophage triglyceride accumulation, macrophage TG biosynthesis, microsomal DGAT1 activity and macrophages oxidative stress, under high glucose concentrations, and this protective effect may be mediated by Pon2 through the attenuation of NADPH-oxidase activity.
Journal ArticleDOI
Specific Amino Acids Affect Cardiovascular Diseases and Atherogenesis via Protection against Macrophage Foam Cell Formation: Review Article.
TL;DR: Screening for anti- or pro-atherogenic amino acids in the macrophage model system showed that glycine, cysteine, alanine, leucine, glutamate, and glutamine significantly affected macrophages atherogenicity mainly through modulation of the cellular triglyceride metabolism.