23 Papers
431 Citations
Irit Maor is an academic researcher from Technion – Israel Institute of Technology. The author has contributed to research in topics: Lipoprotein & Cholesterol. The author has an hindex of 16, co-authored 21 publications. Previous affiliations of Irit Maor include Rappaport Faculty of Medicine.
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Papers
Oxidized low density lipoprotein leads to macrophage accumulation of unesterified cholesterol as a result of lysosomal trapping of the lipoprotein hydrolyzed cholesteryl ester.
Irit Maor,Michael Aviram +1 more
TL;DR: It is concluded that upon incubation of macrophages with Ox-LDL, lysosomal hydrolysis of the lipoprotein CE is not impaired but cellular accumulation of the Ox- LDL-derived UC occurs as a result of trapping of the hydrolyzed CE in the macrophage lysOSomal compartment which may be related to the effect of oxysterols in Ox-ldL.
90
Lesioned low density lipoprotein in atherosclerotic apolipoprotein E-deficient transgenic mice and in humans is oxidized and aggregated.
Michael Aviram,Irit Maor,Shlomo Keidar,Tony Hayek,J. Oiknine,Yaron Bar-El,Zvi Adler,Victor Kertzman,Simcha Milo +8 more
TL;DR: Both oxidation and aggregation of lesioned LDL could be the result of aortic lesioned-induced modification of the lipoprotein, and both of these modified forms of LDL can further contribute to the acceleration of the atherosclerotic process.
89
Plasma LDL Oxidation Leads to Its Aggregation in the Atherosclerotic Apolipoprotein E-Deficient Mice
TL;DR: It is concluded that in E degree mice, LDL oxidation, which already took place in the plasma, can lead to the lipoprotein aggregation, and the use of an appropriate antioxidant can inhibit the formation of both atherogenic forms of LDL.
89
Oxidized monocyte-derived macrophages in aortic atherosclerotic lesion from apolipoprotein E-deficient mice and from human carotid artery contain lipid peroxides and oxysterols.
TL;DR: The present study demonstrated the presence of lipid-peroxidized monocytes already in the blood, which are further oxidized in the arterial wall after their conversion into macrophages, which could be considered key contributors to foam cell formation, the hallmark of early atherosclerosis.
82
Pravastatin inhibits cellular cholesterol synthesis and increases low density lipoprotein receptor activity in macrophages : in vitro and in vivo studies
TL;DR: The results indicate that the selective uptake of pravastatin shown for hepatocytes can be extended to macrophages.