Medizinische Klinik mit Schwerpunkt Kardiologie und Angiologie, Charité-Universitätsmedizin Berlin, Charitéplatz 1, Campus Mitte, D-10117 Berlin, Germany.
Cardiovasc Res. 2010 Jan 15;85(2):281-90. doi: 10.1093/cvr/cvp315. Epub 2009 Sep 17.
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.
泛素-蛋白酶体系统（UPS）已被认为是心血管疾病的关键调节途径。尽管该系统在血管内皮功能障碍发病机制中的作用在很大程度上仍不清楚，但现有数据表明，蛋白酶体活性可被涉及内皮功能调节的介质和过程（如一氧化氮和氧化应激）所改变。此外，有一些证据表明 UPS 本身调节血管稳态的关键酶内皮型一氧化氮合酶的活性，与参与内皮功能调节的其他血管活性介质相互作用，影响血管内氧化应激反应，从而有助于调节内皮（功能）障碍。这篇综述讨论了 UPS 在血管内皮功能障碍中的潜在意义。
