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HIV Protease Inhibitors‐induced Atherosclerosis: Prevention by α‐Tocopherol
Author(s) -
Munteanu Adelina,
Ricciarelli Roberta,
Zingg JeanMarc
Publication year - 2004
Publication title -
iubmb life
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.132
H-Index - 113
eISSN - 1521-6551
pISSN - 1521-6543
DOI - 10.1080/15216540400020387
Subject(s) - cd36 , ritonavir , scavenger receptor , protease , pharmacology , proteasome , downregulation and upregulation , drug , tocopherol , in vitro , medicine , human immunodeficiency virus (hiv) , chemistry , biology , immunology , antioxidant , cholesterol , biochemistry , receptor , enzyme , antiretroviral therapy , vitamin e , viral load , lipoprotein , gene
Prolonged treatments with inhibitors of human immunodeficiency (HIV)‐encoded protease (ARPI) have been reported to induce early atherosclerotic events. Our in vitro study indicates that α‐tocopherol may prevent drug‐induced premature atherosclerosis since it interferes with CD36 scavenger receptor over‐expression induced by ritonavir in monocytes. The mechanism of CD36 upregulation by ritonavir involves inhibition of the ubiquitin‐proteasome system and α‐tocopherol is able to normalize proteasome activity. These findings suggest that ARPI combined with early α‐tocopherol supplementation may decrease the drug‐induced atherosclerotic risk.IUBMB Life, 56: 629‐631, 2004