The modification of nuclear, cytoplasmic, and mitochondrial proteins by O-linked β-N-actylglucosamine (O-GlcNAc) is an essential posttranslational modification that is common in metozoans. O-GlcNAc is cycled on and off proteins in response to environmental and physiological stimuli impacting protein function, which, in turn, tunes pathways that include transcription, translation, proteostasis, signal transduction, and metabolism. One class of stimulus that induces rapid and dynamic changes to O-GlcNAc is cellular injury, resulting from environmental stress (for instance, heat shock), hypoxia/reoxygenation injury, ischemia reperfusion injury (heart attack, stroke, trauma hemorrhage), and sepsis. Acute elevation of O-GlcNAc before or after injury reduces apoptosis and necrosis, suggesting that injury-induced changes in O-GlcNAcylation regulate cell fate decisions. However, prolonged elevation or reduction in O-GlcNAc leads to a maladaptive response and is associated with pathologies such as hypertrophy and heart failure. In this review, we discuss the impact of O-GlcNAc in both acute and prolonged models of injury with a focus on the heart and biological mechanisms that underpin cell survival.

中文翻译：

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细胞内糖基化在细胞保护和心脏病中的多方面作用


O-连接 β-N-乙酰氨基葡萄糖 (O-GlcNAc) 对细胞核、细胞质和线粒体蛋白的修饰是后生动物中常见的重要翻译后修饰。 O-GlcNAc 在蛋白质上循环，以响应影响蛋白质功能的环境和生理刺激，进而调节转录、翻译、蛋白质稳态、信号转导和代谢等途径。引起 O-GlcNAc 快速动态变化的一类刺激是细胞损伤，由环境应激（例如热休克）、缺氧/复氧损伤、缺血再灌注损伤（心脏病发作、中风、创伤出血）和败血症引起。损伤前后 O-GlcNAc 的急性升高会减少细胞凋亡和坏死，这表明损伤诱导的 O-GlcNAc 化变化调节细胞命运决定。然而，O-GlcNAc 的长期升高或降低会导致适应不良反应，并与肥厚和心力衰竭等病理相关。在这篇综述中，我们讨论了 O-GlcNAc 在急性和长期损伤模型中的影响，重点关注心脏和支持细胞存活的生物机制。