Lipoprotein sialylation in atherosclerosis: Lessons from mice.
Lipoprotein sialylation in atherosclerosis: Lessons from mice.
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DOI：
10.3389/fendo.2022.953165
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发表时间：
2022
影响因子：
5.2
通讯作者：
中科院分区：
文献类型：
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唾液酸化是一种动态调节的修饰，通常发生在真核细胞中糖蛋白和糖脂的聚糖链末端。唾液酸化通过调节蛋白质-蛋白质相互作用、细胞内定位、囊泡运输和信号转导在广泛的生物过程中起关键作用。大多数参与脂蛋白代谢和动脉粥样硬化形成的蛋白质，如载脂蛋白和脂蛋白受体，在其聚糖结构中被唾液酸化。早期对人类和临床前模型的研究发现脂蛋白的低唾液酸化与动脉粥样硬化之间存在正相关性。最近在小鼠中使用功能丧失和获得方法的工作揭示了蛋白质唾液酸化因果调节动脉粥样硬化过程的分子和细胞机制。这篇简要综述的目的是总结小鼠模型中的这些发现，并提供脂蛋白唾液酸化和动脉粥样硬化的机制见解。
Sialylation is a dynamically regulated modification, which commonly occurs at the terminal of glycan chains in glycoproteins and glycolipids in eukaryotic cells. Sialylation plays a key role in a wide array of biological processes through the regulation of protein–protein interactions, intracellular localization, vesicular trafficking, and signal transduction. A majority of the proteins involved in lipoprotein metabolism and atherogenesis, such as apolipoproteins and lipoprotein receptors, are sialylated in their glycan structures. Earlier studies in humans and in preclinical models found a positive correlation between low sialylation of lipoproteins and atherosclerosis. More recent works using loss- and gain-of-function approaches in mice have revealed molecular and cellular mechanisms by which protein sialylation modulates causally the process of atherosclerosis. The purpose of this concise review is to summarize these findings in mouse models and to provide mechanistic insights into lipoprotein sialylation and atherosclerosis.