Atherosclerosis is the primary underlying cause of myocardial infarction and stroke. Atherosclerotic cardiovascular disease is characterized by a chronic inflammatory reaction in medium-to-large-sized arteries, with its onset and perpetuation driven by leukocytes infiltrating the subendothelial space. Activation of endothelial cells triggered by hyperlipidaemia and lipoprotein retention in the arterial intima initiates the accumulation of pro-inflammatory leukocytes in the arterial wall, fostering the progression of atherosclerosis. This inflammatory response is coordinated by an array of soluble mediators, namely cytokines and chemokines, that amplify inflammation both locally and systemically and are complemented by tissue-specific molecules that regulate the homing, adhesion and transmigration of leukocytes. Despite abundant evidence from mouse models, only a few therapies targeting leukocytes in atherosclerosis have been assessed in humans. The major challenges for the clinical translation of these therapies include the lack of tissue specificity and insufficient selectivity of inhibition strategies. In this Review, we discuss the latest research on receptor–ligand pairs and interactors that regulate leukocyte influx into the inflamed artery wall, primarily focusing on studies that used pharmacological interventions. We also discuss mechanisms that promote the resolution of inflammation and highlight how major findings from these research areas hold promise as potential therapeutic strategies for atherosclerotic cardiovascular disease.

动脉粥样硬化是心肌梗死和中风的主要原因。动脉粥样硬化性心血管疾病的特征是中大型动脉的慢性炎症反应，其发生和持续是由浸润内皮下间隙的白细胞驱动的。由高脂血症和动脉内膜脂蛋白滞留触发的内皮细胞激活启动促炎白细胞在动脉壁中的积累，促进动脉粥样硬化的进展。这种炎症反应由一系列可溶性介质（即细胞因子和趋化因子）协调，这些介质在局部和全身放大炎症，并辅以调节白细胞归巢、粘附和迁移的组织特异性分子。尽管小鼠模型有大量证据，但只有少数针对动脉粥样硬化白细胞的疗法在人类中进行了评估。这些疗法临床转化的主要挑战包括缺乏组织特异性和抑制策略的选择性不足。在这篇综述中，我们讨论了关于调节白细胞流入发炎动脉壁的受体-配体对和相互作用物的最新研究，主要集中在使用药物干预的研究。我们还讨论了促进炎症消退的机制，并强调了这些研究领域的主要发现如何有望成为动脉粥样硬化性心血管疾病的潜在治疗策略。