PDF(Pubmed)
Abstract：
Protein posttranslational modifications are important factors that mediate the fine regulation of signaling molecules. O-linked β-N-acetylglucosamine-modification (O-GlcNAcylation) is a monosaccharide modification on N-acetylglucosamine linked to the hydroxyl terminus of serine and threonine of proteins. O-GlcNAcylation is responsive to cellular stress as a reversible and posttranslational modification of nuclear, mitochondrial and cytoplasmic proteins. Mitochondrial proteins are the main targets of O-GlcNAcylation and O-GlcNAcylation is a key regulator of mitochondrial homeostasis by directly regulating the mitochondrial proteome or protein activity and function. Disruption of O-GlcNAcylation is closely related to mitochondrial dysfunction. More importantly, the O-GlcNAcylation of cardiac proteins has been proven to be protective or harmful to cardiac function. Mitochondrial homeostasis is crucial for cardiac contractile function and myocardial cell metabolism, and the imbalance of mitochondrial homeostasis plays a crucial role in the pathogenesis of cardiovascular diseases (CVDs). In this review, we will focus on the interactions between protein O-GlcNAcylation and mitochondrial homeostasis and provide insights on the role of mitochondrial protein O-GlcNAcylation in CVDs.
摘要：
蛋白质翻译后修饰是介导信号分子精细调节的重要因素。O-连接的β-N-乙酰葡糖胺修饰（O-GlcNAcylation）是对与蛋白质的丝氨酸和苏氨酸的羟基末端连接的N-乙酰葡糖胺的单糖修饰。O-GlcNAcylation是对细胞应激的响应，作为核的可逆和翻译后修饰，线粒体和细胞质蛋白。线粒体蛋白质是O-GlcNAcylation的主要靶标，O-GlcNAcylation通过直接调节线粒体蛋白质组或蛋白质的活性和功能，是线粒体稳态的关键调节因子。O-GlcNAcylation的破坏与线粒体功能障碍密切相关。更重要的是,心脏蛋白的O-GlcNAcylation已被证明对心脏功能具有保护作用或有害作用。线粒体稳态对心脏收缩功能和心肌细胞代谢至关重要，线粒体稳态的失衡在心血管疾病（CVD）的发病机制中起着至关重要的作用。在这次审查中,我们将专注于蛋白质O-GlcNAcylation与线粒体稳态之间的相互作用，并提供有关线粒体蛋白质O-GlcNAcylation在CVD中的作用的见解。
