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首页> 外文期刊>Current opinion in lipidology >Mechanisms of leukocyte recruitment to atherosclerotic lesions: future prospects.
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Mechanisms of leukocyte recruitment to atherosclerotic lesions: future prospects.

机译：白细胞募集到动脉粥样硬化病变的机制：未来前景。

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PURPOSE OF REVIEW: Leukocyte invasion in the arterial wall is critical in the development of atherosclerotic lesions. This review describes recent advances in the understanding of leukocyte recruitment in atherogenesis and in the development of vulnerable plaque. It also discusses limitations in the current knowledge of this process and how these limitations may be addressed. RECENT FINDINGS: The adhesive function of platelets has recently been highlighted as an important recruitment mechanism in atherosclerosis. For example, targeted deficiency of P-selectin in platelets reduces atherosclerosis in mice. Platelets also increase monocyte recruitment in atherosclerosis by secreting chemokines such as platelet factor 4 (CXCL4) or RANTES (CCL5), which trigger monocyte arrest in atherosclerotic arteries. A causal role for RANTES in atherosclerosis was shown by a protective effect of the blockage of RANTES receptors in apolipoprotein E-deficient mice. A similar effect was also demonstrated for the fractalkine receptor CX3CR1. Moreover, the classic chemoattractant LTB4 plays important roles in atherosclerosis, inasmuch as the absence of the principal LTB4 receptor (BLT1) reduces early atherosclerosis in mice. Novel data have also shown that many types of cells in lesions express 5-lipoxygenase, which indicates a rich source of leukotrienes in plaque. SUMMARY: Recent data provide evidence for the involvement of several adhesive and signalling mechanisms in leukocyte recruitment in atherosclerosis. However, the specific mechanisms that are responsible for the accumulation of proatherogenic leukocytes in lesions are unclear. Detailed study of certain subclasses of leukocytes in the recruitment process will be important in future studies in this field.
机译：审查目的：白细胞在动脉壁的侵袭对动脉粥样硬化病变的发展至关重要。这篇综述描述了在动脉粥样硬化中白细胞募集的理解以及易损斑块的发展方面的最新进展。它还讨论了该过程的当前知识中的限制以及如何解决这些限制。最近的发现：血小板的黏附功能最近被认为是动脉粥样硬化的重要募集机制。例如，血小板中P-选择蛋白的靶向缺乏可降低小鼠的动脉粥样硬化。血小板还通过分泌趋化因子（如血小板因子4（CXCL4）或RANTES（CCL5））触发动脉粥样硬化动脉中的单核细胞停滞，从而增加单核细胞在动脉粥样硬化中的募集。 RANTES在载脂蛋白E缺陷型小鼠中的阻断作用显示了RANTES在动脉粥样硬化中的因果作用。分数链烷烃受体CX3CR1也表现出相似的作用。此外，经典的化学引诱剂LTB4在动脉粥样硬化中起重要作用，因为缺乏主要的LTB4受体（BLT1）可以减轻小鼠的早期动脉粥样硬化。新数据还表明，病变中的许多类型的细胞都表达5-脂氧合酶，这表明噬菌斑中有丰富的白三烯来源。摘要：最新数据为动脉粥样硬化白细胞募集中几种粘附和信号传导机制的参与提供了证据。然而，尚不清楚引起病变部位促动脉粥样硬化白细胞积累的具体机制。在募集过程中对某些白细胞亚类的详细研究对于该领域的未来研究将是重要的。

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