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Apolipoprotein M: Bridging HDL and endothelial function

机译:载脂蛋白M:桥接HDL和内皮功能

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Purpose of review: The review will address the potential roles of apolipoprotein M (apoM) as a carrier protein and modulator of sphingosine-1-phosphate (S1P) bioactivity. Recent findings: Recombinant apoM can bind small lipids such as retinoic acid, oxidized phospholipids, and S1P. Thus, the effects of apoM may be pleiotrophic. The S1P binding ability of apoM has biological impact. ApoM-bound S1P can activate S1P1 receptors on endothelial cells and deficiency of apoM abolishes the presence of S1P in HDL. In mice, the lack of apoM causes dysfunctional endothelial barrier function in the lungs. In humans, sepsis that is characterized by impaired endothelial function is associated with low plasma apoM. Summary: Plasma apoM is mainly bound to HDL. The roles of apoM in atherosclerosis and lipoprotein metabolism have been given much attention. New in the field is the discovery of apoM as a chaperone for S1P. S1P is a bioactive lipid with effects on angiogenesis, lymphocyte trafficking, endothelial cell migration, and inflammation. A drug targeting the S1P-system (fingolimod) is now used for treatment of multiple sclerosis. It improves the blood-brain barrier and inhibits migration of lymphocytes into the brain. Further exploration of the apoM/S1P axis may uncover its potential as a biomarker and target for new treatments.
机译:审查目的:审查将探讨载脂蛋白M(apoM)作为载体蛋白和鞘氨醇-1-磷酸(S1P)生物活性调节剂的潜在作用。最近的发现:重组apoM可以结合小脂质,例如视黄酸,氧化的磷脂和S1P。因此,apoM的作用可能是多营养的。 apoM的S1P结合能力具有生物学影响。 ApoM结合的S1P可以激活内皮细胞上的S1P1受体,而apoM的缺乏则消除了HDL中S1P的存在。在小鼠中,缺乏apoM会导致肺内皮功能障碍。在人类中,以内皮功能受损为特征的脓毒症与低血浆apoM有关。简介:血浆apoM主要与HDL结合。 apoM在动脉粥样硬化和脂蛋白代谢中的作用已受到广泛关注。该领域的新发现是apoM作为S1P的伴侣。 S1P是一种生物活性脂质,可影响血管生成,淋巴细胞运输,内皮细胞迁移和炎症。现在,针对S1P系统的药物(芬戈莫德)已用于治疗多发性硬化症。它改善了血脑屏障,并抑制了淋巴细胞向大脑的迁移。对apoM / S1P轴的进一步探索可能会发现其作为生物标志物和新疗法靶标的潜力。

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