Atherosclerosis is a long-term, chronic inflammatory disease of the vessel wall leading to the formation of occlusive or rupture-prone lesions in large arteries. Complications of atherosclerosis can become severe and lead to cardiovascular diseases (CVD) with lethal consequences. During the last three decades, chemokines and their receptors earned great attention in the research of atherosclerosis as they play a key role in development and progression of atherosclerotic lesions. They orchestrate activation, recruitment, and infiltration of immune cells and subsequent phenotypic changes, e.g., increased uptake of oxidized low-density lipoprotein (oxLDL) by macrophages, promoting the development of foam cells, a key feature developing plaques. In addition, chemokines and their receptors maintain homing of adaptive immune cells but also drive pro-atherosclerotic leukocyte responses. Recently, specific targeting, e.g., by applying cell specific knock out models have shed new light on their functions in chronic vascular inflammation. This article reviews recent findings on the role of immunomodulatory chemokines in the development of atherosclerosis and their potential for targeting.

中文翻译：

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动脉粥样硬化中的炎症趋化因子

动脉粥样硬化是血管壁的长期慢性炎症性疾病，导致大动脉中形成闭塞性或易破裂病变。动脉粥样硬化的并发症可能会变得严重并导致心血管疾病 (CVD) 并具有致命后果。在过去的 30 年中，趋化因子及其受体在动脉粥样硬化的研究中获得了极大的关注，因为它们在动脉粥样硬化病变的发展和进展中起着关键作用。它们协调免疫细胞的激活、募集和浸润以及随后的表型变化，例如，巨噬细胞对氧化低密度脂蛋白 (oxLDL) 的吸收增加，促进泡沫细胞的发育，这是形成斑块的关键特征。此外，趋化因子及其受体维持适应性免疫细胞的归巢，但也驱动促动脉粥样硬化的白细胞反应。最近，特定的靶向，例如，通过应用细胞特异性敲除模型，揭示了它们在慢性血管炎症中的功能。本文回顾了最近关于免疫调节趋化因子在动脉粥样硬化发展中的作用及其靶向潜力的发现。