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巨噬细胞驱动的外泌体调节心血管疾病的进展。

Macrophage-driven exosomes regulate the progression of cardiovascular disease.

作者信息

Qi Liao, Luo De-Zhu, Li HuLi, Yan JianWen, He WenJie

机构信息

Pengzhou Hospital of Traditional Chinese Medicine, Pengzhou, China.

Department of Anesthesiology, West China Hospital of Sichuan University, Chengdu, Sichuan, China.

出版信息

Front Pharmacol. 2025 Apr 30;16:1563800. doi: 10.3389/fphar.2025.1563800. eCollection 2025.

DOI:10.3389/fphar.2025.1563800
PMID:40371346
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12075947/
Abstract

Exosomes, as vital mediators of intercellular communication, play a critical role in the progression of cardiovascular disease (CVD). Recently, macrophage-derived exosomes (Mφ-Exos) have garnered increasing attention because of their significant potential in early diagnosis, pathological processes, and therapeutic applications for CVD. Exosomes contain diverse nucleic acids (e.g., miRNAs, mRNAs, and long noncoding RNAs (lncRNAs)) and proteins, which serve as specific biomarkers that regulate various stages of CVD. For example, miRNAs encapsulated within exosomes (e.g., miR-21, miR-133a, and miR-155) are closely associated with atherosclerosis, myocardial infarction, coronary artery disease, and stroke, and changes in their abundance can serve as diagnostic and prognostic indicators. Additionally, the composition of Mφ-Exos, including miRNAs, lipids, and proteins, plays a significant role in the initiation, progression, and inflammation of CVD. Research on Mφ-Exos provides new directions for early diagnosis, mechanistic exploration, and novel therapeutic targets in CVD. However, challenges remain regarding exosome isolation and identification technologies. Future studies need to further explore the biological properties of exosomes and develop more efficient, economical, and straightforward isolation methods. This review summarizes the multifaceted regulatory roles of Mφ-Exos in CVD, encompassing key processes such as inflammation, angiogenesis, metabolism, and cell death. Research has shown that M1-Exos promote the progression and exacerbation of CVD through pro-inflammatory and pro-fibrotic mechanisms, while M2-Exos demonstrate significant therapeutic potential via anti-inflammatory, pro-angiogenic, and metabolic reprogramming pathways. These findings not only reveal the complex mechanisms of Mφ-Exos in CVD but also provide new perspectives and potential targets for early diagnosis and precision treatment of the disease.

摘要

外泌体作为细胞间通讯的重要介质,在心血管疾病(CVD)的进展中起关键作用。近年来,巨噬细胞衍生的外泌体(Mφ-Exos)因其在CVD的早期诊断、病理过程及治疗应用方面的巨大潜力而受到越来越多的关注。外泌体包含多种核酸(如微小RNA、信使RNA和长链非编码RNA)和蛋白质,它们作为特定的生物标志物,调节CVD的各个阶段。例如,外泌体中包裹的微小RNA(如miR-21、miR-133a和miR-155)与动脉粥样硬化、心肌梗死、冠状动脉疾病和中风密切相关,其丰度的变化可作为诊断和预后指标。此外,Mφ-Exos的组成,包括微小RNA、脂质和蛋白质,在CVD的起始、进展和炎症中起重要作用。对Mφ-Exos的研究为CVD的早期诊断、机制探索和新的治疗靶点提供了新方向。然而,在外泌体分离和鉴定技术方面仍存在挑战。未来的研究需要进一步探索外泌体的生物学特性,并开发更高效、经济和简便的分离方法。本综述总结了Mφ-Exos在CVD中的多方面调节作用,包括炎症、血管生成、代谢和细胞死亡等关键过程。研究表明,M1-Exos通过促炎和促纤维化机制促进CVD的进展和恶化,而M2-Exos通过抗炎、促血管生成和代谢重编程途径显示出显著的治疗潜力。这些发现不仅揭示了Mφ-Exos在CVD中的复杂机制,也为该疾病的早期诊断和精准治疗提供了新的视角和潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a8/12075947/d0b3172ddbe2/fphar-16-1563800-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a8/12075947/1e60d3728a87/fphar-16-1563800-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a8/12075947/9f949aaf56b9/fphar-16-1563800-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a8/12075947/1a5563b7beb4/fphar-16-1563800-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a8/12075947/982c46436285/fphar-16-1563800-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a8/12075947/d0b3172ddbe2/fphar-16-1563800-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a8/12075947/1e60d3728a87/fphar-16-1563800-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a8/12075947/9f949aaf56b9/fphar-16-1563800-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a8/12075947/1a5563b7beb4/fphar-16-1563800-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a8/12075947/982c46436285/fphar-16-1563800-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e5a8/12075947/d0b3172ddbe2/fphar-16-1563800-g005.jpg

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本文引用的文献

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