O-GlcNAc signaling in the cardiovascular system.
O-GlcNAc signaling in the cardiovascular system.
复制标题
DOI：
10.1161/circresaha.110.224675
复制
发表时间：
2010-07-23
影响因子：
20.1
通讯作者：
Jones SP
中科院分区：
文献类型：
--
作者：
Ngoh GA;Facundo HT;Zafir A;Jones SP
Cardiovascular function is regulated at multiple levels. Some of the most important aspects of such regulation involve alterations in an ever-growing list of post-translational modifications. One such modification orchestrates input from numerous metabolic cues to modify proteins and alter their localization and/or function. Known as the beta-O-linkage of N-acetylglucosamine (i.e. O-GlcNAc) to cellular proteins, this unique monosaccharide is involved in a diverse array of physiologic and pathologic functions. This Review will introduce readers to the general concepts related to O-GlcNAc, the regulation of this modification, and its role in primary pathophysiology. Much of the existing literature regarding the role of O-GlcNAcylation in disease addresses the protracted elevations in O-GlcNAcylation observed during diabetes. In this Review, we will focus on the emerging evidence of its involvement in the cardiovascular system. In particular, we will highlight evidence of protein O-GlcNAcylation as an autoprotective alarm or stress response. We will discuss recent literature supporting the idea that promoting O-GlcNAcylation improves cell survival during acute stress (e.g. hypoxia, ischemia, oxidative stress), whereas limiting O-GlcNAcylation exacerbates cell damage in similar models. In addition to addressing the potential mechanisms of O-GlcNAc-mediated cardioprotection, we will discuss technical issues related to studying protein O-GlcNAcylation in biological systems. The reader should gain an understanding of what protein O-GlcNAcylation is, and, that its roles in the acute and chronic disease settings appear distinct.
