Skip Navigation

European Heart Journal 1990 11(Supplement E):122-127; doi:10.1093/eurheartj/11.suppl_E.122
Copyright © 1990 by the European Society of Cardiology.
This Article
Right arrow Full Text (PDF)
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Kita, T.
Right arrow Articles by Kawai, C.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kita, T.
Right arrow Articles by Kawai, C.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© 1990 The European Society of Cardiology

The role of oxidized low density lipoprotein in the pathogenesis of atherosclerosis

T. Kita*,, K. Ishii*, M. Yokode{dagger},{ddagger}, N. Kume{ddagger}, Y. Nagano*, H. Arai{ddagger} and C. Kawai{ddagger}

* Department of Geriatric Medicine, Faculty of Medicine, Kyoto University Japan
{dagger} University of Texas Southwestern Medical Center at Dallas USA
{ddagger} Department of Internal Medicine, 3rd Division, Faculty of Medicine, Kyoto University Japan

Address for correspondence: Prof. Toru Kita, Department of Geriatric Medicine, Faculty of Medicine, Kyoto University. 54 Kawaracho Shogoin, Sakyeh-ku, Kyoto 606, Japan

Recently, it has been suggested that oxidized low density lipoprotein (LDL) plays an important role in atherogenesis by facilitating the accumulation of lipids in macrophages. In vitro studies from our laboratory have shown that oxidized LDL is recognized not only by a specific receptor, but also by a receptor which recognizes both oxidized LDL and acetyl LDL. Probucol, originally developed as an antioxidant, prevents the oxidative modification of LDL in vitro. Our recent studies show that probucol prevents the progression of atherosclerosis in homozygour WHHL rabbits in vivo without any changes in plasma LDL cholesterol levels.

These results strongly suggest that oxidative modification of LDL could occur in vivo and probucol could slow the progression of atherosclerosis, especially the foam cell-rich fatty streak lesions, without changing plasma cholesterol levels.

Key Words: WHHL rabbit • atherosclerosis • oxidized LDL • receptor


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.