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高密度脂蛋白和 microRNAs。

HDL and microRNAs.

机构信息

Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital, NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing, China.

School of Bioscience and Technology, Weifang Medical University, Weifang, Shandong, China.

出版信息

Adv Exp Med Biol. 2022;1377:153-161. doi: 10.1007/978-981-19-1592-5_12.

DOI:10.1007/978-981-19-1592-5_12
PMID:35575928
Abstract

In previous chapters, we know that high-density lipoproteins (HDLs) could act at multiple cell lines and then trigger intracellular molecular pathway to prevent several metabolic diseases. Besides the classic genes regulating cholesterol efflux and reverse cholesterol transport (RCT), microRNAs (miRNAs) could also affect HDLs biogenesis, metabolism, and functions. This chapter summarizes the miRNAs, which regulate HDLs functions in table. In addition, HDLs are good vectors for miRNAs. They could carry miRNAs in circulation and take them into several cells such as macrophages and endothelial cells. Complete understanding of the miRNAs associated with HDL regulation would give us broader insights to prevent and treat metabolic diseases.

摘要

在前面的章节中,我们知道高密度脂蛋白(HDL)可以在多种细胞系中发挥作用,然后触发细胞内分子途径来预防多种代谢疾病。除了经典的调节胆固醇外排和胆固醇逆转运(RCT)的基因外,微小 RNA(miRNA)也可以影响 HDL 的生成、代谢和功能。本章总结了表中调节 HDL 功能的 miRNA。此外,HDL 是 miRNA 的良好载体。它们可以在循环中携带 miRNA,并将其带入巨噬细胞和内皮细胞等多种细胞。对与 HDL 调节相关的 miRNA 的全面了解将使我们更深入地了解预防和治疗代谢疾病的方法。

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本文引用的文献

1
Diabetic Nephropathy Alters the Distribution of Circulating Angiogenic MicroRNAs Among Extracellular Vesicles, HDL, and Ago-2.糖尿病肾病改变了循环血管生成 microRNAs 在细胞外囊泡、高密度脂蛋白和 Ago-2 中的分布。
Diabetes. 2019 Dec;68(12):2287-2300. doi: 10.2337/db18-1360. Epub 2019 Sep 10.
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High dose rosuvastatin increases ABCA1 transporter in human atherosclerotic plaques in a cholesterol-independent fashion.高剂量瑞舒伐他汀以胆固醇非依赖方式增加人动脉粥样硬化斑块中的 ABCA1 转运体。
Int J Cardiol. 2020 Jan 15;299:249-253. doi: 10.1016/j.ijcard.2019.07.094. Epub 2019 Aug 3.
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Specific Disruption of Abca1 Targeting Largely Mimics the Effects of miR-33 Knockout on Macrophage Cholesterol Efflux and Atherosclerotic Plaque Development.
ABCA1 靶向特异性缺失在很大程度上模拟了 miR-33 敲除对巨噬细胞胆固醇流出和动脉粥样硬化斑块形成的影响。
Circ Res. 2019 Mar 15;124(6):874-880. doi: 10.1161/CIRCRESAHA.118.314415.
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MicroRNA-23a-5p promotes atherosclerotic plaque progression and vulnerability by repressing ATP-binding cassette transporter A1/G1 in macrophages.MicroRNA-23a-5p 通过抑制巨噬细胞中的 ATP 结合盒转运蛋白 A1/G1 促进动脉粥样硬化斑块的进展和不稳定性。
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Apoptotic cell induction of miR-10b in macrophages contributes to advanced atherosclerosis progression in ApoE-/- mice.miR-10b 通过诱导巨噬细胞凋亡促进 ApoE-/- 小鼠动脉粥样硬化的进展。
Cardiovasc Res. 2018 Nov 1;114(13):1794-1805. doi: 10.1093/cvr/cvy132.
6
Identification of miR-9-5p as direct regulator of ABCA1 and HDL-driven reverse cholesterol transport in circulating CD14+ cells of patients with metabolic syndrome.鉴定 miR-9-5p 作为代谢综合征患者循环 CD14+细胞中 ABCA1 和 HDL 驱动的胆固醇逆转运的直接调节因子。
Cardiovasc Res. 2018 Jul 1;114(8):1154-1164. doi: 10.1093/cvr/cvy077.
7
MicroRNA-24 aggravates atherosclerosis by inhibiting selective lipid uptake from HDL cholesterol via the post-transcriptional repression of scavenger receptor class B type I.MicroRNA-24 通过抑制清道夫受体 B 类 I 的转录后抑制从高密度脂蛋白胆固醇中选择性摄取脂质,从而加剧动脉粥样硬化。
Atherosclerosis. 2018 Mar;270:57-67. doi: 10.1016/j.atherosclerosis.2018.01.045. Epub 2018 Feb 4.
8
Macrophage deficiency of miR-21 promotes apoptosis, plaque necrosis, and vascular inflammation during atherogenesis.巨噬细胞中 miR-21 的缺失促进动脉粥样硬化形成过程中的细胞凋亡、斑块坏死和血管炎症。
EMBO Mol Med. 2017 Sep;9(9):1244-1262. doi: 10.15252/emmm.201607492.
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MicroRNA-20a/b regulates cholesterol efflux through post-transcriptional repression of ATP-binding cassette transporter A1.MicroRNA-20a/b 通过对 ATP 结合盒转运蛋白 A1 的转录后抑制调节胆固醇外排。
Biochim Biophys Acta Mol Cell Biol Lipids. 2017 Sep;1862(9):929-938. doi: 10.1016/j.bbalip.2017.06.002. Epub 2017 Jun 8.
10
The persistence of low-grade inflammatory monocytes contributes to aggravated atherosclerosis.低水平炎性单核细胞的持续存在导致动脉粥样硬化加重。
Nat Commun. 2016 Nov 8;7:13436. doi: 10.1038/ncomms13436.