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Cardiovascular Research Advance Access first published online on September 17, 2009
This version [Corrected Proof] published online on October 13, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp315
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

The ubiquitin proteasome pathway and endothelial (dys)function

Karl Stangl* and Verena Stangl

Medizinische Klinik mit Schwerpunkt Kardiologie und Angiologie, Charité—Universitätsmedizin Berlin, Charitéplatz 1, Campus Mitte, D-10117 Berlin, Germany

* Corresponding author. Tel: +49 30 450 513 153, Fax: +49 30 450 513 932, Email: karl.stangl{at}charite.de

The ubiquitin proteasome system (UPS) has been recognized as a key regulatory pathway in cardiovascular diseases. Although the role of this system in the pathogenesis of endothelial dysfunction remains largely unknown, available data suggest that proteasome activity is modified by mediators and processes—e.g. nitric oxide and oxidative stress—involved in the regulation of endothelial function. In addition, there is some evidence that the UPS itself modulates the activity of endothelial nitric oxide synthase, the key enzyme of vascular homeostasis, interacts with other vasoactive mediators involved in regulation of endothelial function, influences oxidative stress response in the vasculature, and thereby contributes to regulation of endothelial (dys)function. This review discusses the potential implications of the UPS in endothelial dysfunction.

KEYWORDS Endothelial function; Endothelial dysfunction; Ubiquitin; Proteasome

Time for primary review: 20 days

{dagger} See List of abbreviations.

This article is part of the Spotlight Issue on: The Role of the Ubiquitin-Proteasome Pathway in Cardiovascular Disease


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