Skip Navigation

Cardiovascular Research 2007 76(1):19-28; doi:10.1016/j.cardiores.2007.05.014
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
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 Grande-Allen, K.J.
Right arrow Articles by Little, P.J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Grande-Allen, K.J.
Right arrow Articles by Little, P.J.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2007, European Society of Cardiology

Glycosaminoglycan synthesis and structure as targets for the prevention of calcific aortic valve disease

K.J. Grande-Allena, N. Osmanb,c, M.L. Ballingerb, H. Dadlanib, S. Marascod and P.J. Littleb,c,*

aDepartment of Bioengineering, Rice University, Houston, TX USA 77005
bCell Biology of Diabetes Laboratory, Baker Heart Research Institute, Melbourne, Victoria, 3004, Australia
cDepartments of Medicine and Immunology, Central and Eastern Clinical School, Alfred Hospital, Monash University, Melbourne, 3004, Victoria, Australia
dDepartment of Cardiothoracic Surgery, Alfred Hospital, Melbourne, Victoria 3004, Australia

*Corresponding author. Cell Biology of Diabetes Laboratory, Baker Heart Research Institute, St. Kilda Rd Central, PO Box 6492, Melbourne Victoria 8008, Australia. Tel.: +61 3 8532 1203; fax: +61 3 8532 1100. peter.little{at}baker.edu.au

Calcific aortic valve disease is frequently driven by ageing and the obesity-associated metabolic syndrome, and the increasing impact of these factors indicates that valve disease will become a cardiovascular disease of considerable significance. This disease is now thought to be an active cell-based disease process, which may therefore be amenable to therapeutic intervention. Some similarities are apparent with atherosclerosis. The accumulation of lipid, possibly by retention by proteoglycans and the attraction of inflammatory cells by hyaluronan, may be common to the early stages of both pathologies. The synthesis and structure of glycosaminoglycans, proteoglycans, and hyaluronan are exquisitely regulated, and the signalling pathways controlling these processes may provide tissue-specific opportunities for concomitant prevention of atherosclerosis and calcific aortic valve disease.

KEYWORDS Calcific aortic valve disease; Proteoglycans; Hyaluronan; Lipid retention; Inflammation


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.