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Cardiovascular Research Advance Access originally published online on December 10, 2008
Cardiovascular Research 2009 81(2):242-243; doi:10.1093/cvr/cvn343
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org

Cathepsin K: boon or bale for atherosclerotic plaque stability?

Oliver Hofnagel and Horst Robenek*

Leibniz Institute for Arteriosclerosis Research, 48149 Muenster, Germany

* Corresponding author. Tel: +49 2518 355 6206. E-mail address: robenek@uni-muenster.de

This editorial refers to ‘Leucocyte cathepsin K affects atherosclerotic lesion composition and bone mineral density in low-density lipoprotein receptor deficient mice’ by Guo et al.,4 pp. 278–285, this issue.

The first 10% of the full text of this article appears below.

Cathepsins, cysteine proteases of lysosomes and endosomes, play major physiological roles in general intracellular protein turnover. When they are directed outside the cell, these enzymes also take part in remodelling the extracellular matrix of bone1 and other tissues. Once in the extracellular matrix, the cathepsins degrade elastin and collagen. Since remodelling of the extracellular matrix of arteries is germane to the stabilization of established atherosclerotic plaques, considerable interest is being focused on cathepsins as possible therapeutic targets for plaque stabilization. Undesirable as they may be, atherosclerotic plaques, once formed, have to be maintained in a stable condition to . . . [Full Text of this Article]


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Leucocyte cathepsin K affects atherosclerotic lesion composition and bone mineral density in low-density lipoprotein receptor deficient mice
Jian Guo, Ilze Bot, Ramon de Nooijer, Sandra J. Hoffman, George B. Stroup, Erik A.L. Biessen, G. Martin Benson, Pieter H.E. Groot, Miranda Van Eck, and Theo J.C. Van Berkel
Cardiovasc Res 2009 81: 278-285. [Abstract] [Full Text] [PDF]