Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Am J Physiol Heart Circ Physiol. 2012 May 15;302(10):H1905-18. doi: 10.1152/ajpheart.00445.2011. Epub 2012 Jan 27.
More than 1,000 proteins of the nucleus, cytoplasm, and mitochondria are dynamically modified by O-linked β-N-acetylglucosamine (O-GlcNAc), an essential post-translational modification of metazoans. O-GlcNAc, which modifies Ser/Thr residues, is thought to regulate protein function in a manner analogous to protein phosphorylation and, on a subset of proteins, appears to have a reciprocal relationship with phosphorylation. Like phosphorylation, O-GlcNAc levels change dynamically in response to numerous signals including hyperglycemia and cellular injury. Recent data suggests that O-GlcNAc appears to be a key regulator of the cellular stress response, the augmentation of which is protective in models of acute vascular injury, trauma hemorrhage, and ischemia-reperfusion injury. In contrast to these studies, O-GlcNAc has also been implicated in the development of hypertension and type II diabetes, leading to vascular and cardiac dysfunction. Here we summarize the current understanding of the roles of O-GlcNAc in the heart and vasculature.
细胞核、细胞质和线粒体中的 1000 多种蛋白质都受到 O-连接β-N-乙酰氨基葡萄糖（O-GlcNAc）的动态修饰，这是后生动物中一种必需的翻译后修饰。O-GlcNAc 修饰丝氨酸/苏氨酸残基，被认为以类似于蛋白质磷酸化的方式调节蛋白质功能，并且在蛋白质的一部分上，似乎与磷酸化呈相互关系。与磷酸化一样，O-GlcNAc 水平会根据多种信号（包括高血糖和细胞损伤）而动态变化。最近的数据表明，O-GlcNAc 似乎是细胞应激反应的关键调节剂，在急性血管损伤、创伤性出血和缺血再灌注损伤的模型中，其增强具有保护作用。与这些研究相反，O-GlcNAc 也与高血压和 2 型糖尿病的发展有关，导致血管和心脏功能障碍。在这里，我们总结了目前对 O-GlcNAc 在心脏和血管中的作用的理解。
