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生理激动剂对血小板衍生细胞外囊泡蛋白质组的差异影响。

Differential effects of physiological agonists on the proteome of platelet-derived extracellular vesicles.

机构信息

Division of Cardiology, Medical University of Vienna, Vienna, Austria.

National Heart and Lung Institute, Imperial College London, London, UK.

出版信息

Proteomics. 2024 Aug;24(16):e2400090. doi: 10.1002/pmic.202400090.

DOI:10.1002/pmic.202400090
PMID:39148210
Abstract

Arterial thrombosis contributes to some of the most frequent causes of mortality globally, such as myocardial infarction and stroke. Platelets are essential mediators of physiological haemostasis and pathological thrombosis. Platelet activation is controlled by a multitude of signalling pathways. Upon activation, platelets shed platelet-derived extracellular vesicles (pEVs). In this Special Issue: Extracellular Vesicles, Moon et al. investigate the impact of various platelet agonists (thrombin, ADP, collagen) on the proteome of pEVs. The study demonstrates that pEVs exhibit an agonist-dependent altered proteome compared to their parent cells, with significant variations in proteins related to coagulation, complement, and platelet activation. The study observes the rapid generation of pEVs following agonist stimulation with specific proteome alterations that underscore an active packaging process. This commentary highlights the implications of their findings and discusses the role of pEV cargo in cardiovascular disease with potential novel therapeutic and diagnostic opportunities.

摘要

动脉血栓形成是导致全球一些最常见死亡原因的因素之一,例如心肌梗死和中风。血小板是生理性止血和病理性血栓形成的重要介质。血小板的激活受多种信号通路的控制。激活后,血小板会释放血小板衍生的细胞外囊泡 (pEVs)。在本期《细胞外囊泡特刊》中,Moon 等人研究了各种血小板激动剂(凝血酶、ADP、胶原)对 pEV 蛋白质组的影响。该研究表明,与母细胞相比,pEV 表现出激动剂依赖性改变的蛋白质组,与凝血、补体和血小板激活相关的蛋白质存在显著差异。该研究观察到在激动剂刺激后 pEV 的快速生成,并伴有特定蛋白质组的改变,这突出了一个活跃的包装过程。本评论强调了他们研究结果的意义,并讨论了 pEV 货物在心血管疾病中的作用,以及可能具有新的治疗和诊断机会。

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引用本文的文献

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Extracellular vesicles in atherosclerosis cardiovascular disease: emerging roles and mechanisms.动脉粥样硬化性心血管疾病中的细胞外囊泡:新出现的作用和机制
Front Cardiovasc Med. 2025 Jun 24;12:1611557. doi: 10.3389/fcvm.2025.1611557. eCollection 2025.