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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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.
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Amphiphilic/Bipolar Metallocorroles That Catalyze the Decomposition of Reactive Oxygen and Nitrogen Species, Rescue Lipoproteins from Oxidative Damage, and Attenuate Atherosclerosis in Mice
Adi Haber,Atif Mahammed,Bianca Fuhrman,Nina Volkova,Raymond Coleman,Tony Hayek,Michael Aviram,Zeev Gross +7 more
TL;DR: The motivation for the current investigations was the fact that the particular iron( III) and manganese(III) corroles shown in Scheme 1A were disclosed as potent catalysts for decomposition of peroxynitrite in purely chemical systems, with the former acting very fast and the latter operating through the novel mechanism shown in scheme 1B.
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Macrophage foam cell formation during early atherogenesis is determined by the balance between pro-oxidants and anti-oxidants in arterial cells and blood lipoproteins.
TL;DR: The combination of antioxidants together with active paraoxonase decreases the formation of Ox-LDL and preserves PON1's ability to hydrolyze this atherogenic lipoprotein and hence, to attenuate atherosclerosis.
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Pomegranate juice polyphenols increase recombinant paraoxonase-1 binding to high-density lipoprotein: Studies in vitro and in diabetic patients
TL;DR: It is concluded that oxidative stress impairs binding of fluorescein isothiocyanate-labeled rePon1 to HDL and PJ polyphenols directly increase the HDL-rePON1 association beyond their antioxidative effect.
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Increased Uptake of LDL by Oxidized Macrophages is the Result of an Initial Enhanced LDL Receptor Activity and of a Further Progressive Oxidation of LDL
TL;DR: Increased uptake of LDL by oxidized macrophages results from two routes: enhanced uptake via the LDL receptor due to increased LDL receptor activity; and lipoprotein uptake through the Ox-LDL receptors due to cellular modification of LDL.