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动脉粥样硬化中的外泌体:在发病机制中的作用及治疗靶点

Exosomes in Atherosclerosis: Role in the Pathogenesis and Targets for Therapy.

作者信息

Dabravolski Siarhei, Sukhorukov Vasily N, Glanz Victor, Pleshko Elizaveta, Orekhov Nikolay, Sobenin Igor

机构信息

Department of Biotechnology Engineering, Braude Academic College of Engineering, Snunit 51, P.O. Box 78, Karmiel 2161002, Israel.

Petrovsky Russian National Center of Surgery, 2 Abrikosovsky Lane, 119991- Moscow, Russia.

出版信息

Curr Med Chem. 2024 May 3. doi: 10.2174/0109298673302220240430173404.


DOI:10.2174/0109298673302220240430173404
PMID:38706365
Abstract

Atherosclerotic cardiovascular disease (ASCVD) is an advanced chronic inflammatory disease and the leading cause of death worldwide. The pathological development of ASCVD begins with atherosclerosis, characterised by a pathological remodelling of the arterial wall, lipid accumulation and build-up of atheromatous plaque. As the disease advances, it narrows the vascular lumen and limits the blood, leading to ischaemic necrosis in coronary arteries. Exosomes are nano-sized lipid vesicles of different origins that can carry many bioactive molecules from their parental cells, thus playing an important role in intercellular communication. The roles of exosomes in atherosclerosis have recently been intensively studied, advancing our understanding of the underlying molecular mechanisms. In this review, we briefly introduce exosome biology and then focus on the roles of exosomes of different cellular origins in atherosclerosis development and progression, functional significance of their cargoes and physiological impact on recipient cells. Studies have demonstrated that exosomes originating from endothelial cells, vascular smooth muscle cells, macrophages, dendritic cells, platelets, stem cells, adipose tissue and other sources play an important role in the atherosclerosis development and progression by affecting cholesterol transport, inflammatory, apoptotic and other aspects of the recipient cells' metabolism. MicroRNAs are considered the most significant type of bioactive molecules transported by exosomes and involved in ASCVD development. Finally, we review the current achievements and limitations associated with the use of exosomes for the diagnosis and treatment of ASCVD.

摘要

动脉粥样硬化性心血管疾病(ASCVD)是一种晚期慢性炎症性疾病,也是全球主要的死亡原因。ASCVD的病理发展始于动脉粥样硬化,其特征是动脉壁的病理重塑、脂质积聚和动脉粥样斑块的形成。随着疾病进展,它会使血管腔变窄并限制血液流动,导致冠状动脉缺血性坏死。外泌体是源自不同细胞的纳米级脂质囊泡,可携带来自其亲代细胞的许多生物活性分子,从而在细胞间通讯中发挥重要作用。外泌体在动脉粥样硬化中的作用最近得到了深入研究,增进了我们对潜在分子机制的理解。在这篇综述中,我们简要介绍外泌体生物学,然后重点关注不同细胞来源的外泌体在动脉粥样硬化发生发展中的作用、其货物的功能意义以及对受体细胞的生理影响。研究表明,源自内皮细胞、血管平滑肌细胞、巨噬细胞、树突状细胞、血小板、干细胞、脂肪组织和其他来源的外泌体,通过影响受体细胞代谢的胆固醇转运、炎症、凋亡等方面,在动脉粥样硬化的发生发展中发挥重要作用。微小RNA被认为是外泌体运输的最重要的一类生物活性分子,并参与ASCVD的发展。最后,我们综述了与使用外泌体诊断和治疗ASCVD相关的当前成果和局限性。

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引用本文的文献

[1]
The Link between Lipids and Inflammation: Focus on Targeting Sialidase Activity as a Novel Strategy for Anti-Atherosclerotic Therapy.

Curr Med Chem. 2025

本文引用的文献

[1]
Exosomes derived from programmed cell death: mechanism and biological significance.

Cell Commun Signal. 2024-3-1

[2]
MCL attenuates atherosclerosis by suppressing macrophage ferroptosis via targeting KEAP1/NRF2 interaction.

Redox Biol. 2024-2

[3]
Adipose tissue‑derived extracellular vesicles: Systemic messengers in health and disease (Review).

Mol Med Rep. 2023-10

[4]
Extracellular vesicles as biomarkers and modulators of atherosclerosis pathogenesis.

Front Cardiovasc Med. 2023-5-26

[5]
Extracellular vesicles arising from apoptosis: forms, functions, and applications.

J Pathol. 2023-8

[6]
Exosomes in Cardiovascular Disease: From Mechanism to Therapeutic Target.

Metabolites. 2023-3-27

[7]
Long noncoding RNAs in cardiovascular disease.

Curr Opin Cardiol. 2023-5-1

[8]
The Landscape of Circular RNAs in Cardiovascular Diseases.

Int J Mol Sci. 2023-2-26

[9]
Exosomal miR-27b-3p secreted by visceral adipocytes contributes to endothelial inflammation and atherogenesis.

Cell Rep. 2023-1-31

[10]
miR-186-5p Dysregulation in Serum Exosomes from Patients with AMI Aggravates Atherosclerosis via Targeting LOX-1.

Int J Nanomedicine. 2022

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