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首页> 外文期刊>Current opinion in lipidology >The role of chemokines in atherosclerosis: recent evidence from experimental models and population genetics.
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The role of chemokines in atherosclerosis: recent evidence from experimental models and population genetics.

机译：趋化因子在动脉粥样硬化中的作用：来自实验模型和群体遗传学的最新证据。

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PURPOSE OF REVIEW: Atherosclerosis is an inflammatory disease process. This review discusses the recent genetic evidence from animal models and human populations that highlight the importance of chemokines in atherosclerosis. RECENT FINDINGS: CC-chemokine/CC-chemokine receptors (CCR), including CCR2/ MCP-1 (monocyte chemoattractant protein-1) and CCR5/RANTES (regulated on activation, normal T-cell expressed and secreted), have been shown in animal knockout and transgenic studies to have significant effects on atherosclerotic lesion size and macrophage recruitment. More recently fractalkine (CX3C1) and its receptor (CX3CR1) have emerged as another important pathway in atherosclerosis. For example, fractalkine is present in human atherosclerotic lesions and is able to stimulate platelet activation and adhesion. CX3CR1 is expressed on human aortic smooth muscle cells and CX3CR1/apolipoprotein E double knockout mice have significantly reduced atherosclerotic lesion size and macrophage recruitment. Human population genetic studies have tried to assess the importance of chemokines in human atherosclerosis. Currently, there is conflicting evidence regarding an association between polymorphisms in CCR2/MCP-1 and CCR5/RANTES and coronary artery disease. There is evidence, however, for an association between the fractalkine receptor polymorphism (CX3CR1-I249) and coronary artery disease in both human population and function studies. SUMMARY: Recent transgenic and gene knockout studies in murine models of atherosclerosis have highlighted the importance of chemokines and their receptors in atherosclerosis. Genetic evidence for a role of chemokines and their receptors in human population studies remains under investigation. Identifying chemokine polymorphisms could help to determine pathways that are important in atherosclerosis disease pathology and that may suggest novel therapeutic targets.
机译：审查目的：动脉粥样硬化是炎性疾病的过程。这篇综述讨论了来自动物模型和人群的最新遗传证据，这些证据突出了趋化因子在动脉粥样硬化中的重要性。最近发现：CC趋化因子/ CC趋化因子受体（CCR），包括CCR2 / MCP-1（单核细胞趋化蛋白-1）和CCR5 / RANTES（受激活调节，正常T细胞表达和分泌）已在动物基因敲除和转基因研究对动脉粥样硬化病变的大小和巨噬细胞募集有重大影响。最近，fractalkine（CX3C1）及其受体（CX3CR1）已成​​为动脉粥样硬化的另一个重要途径。例如，人动脉粥样硬化病变中存在fractalkine，并且能够刺激血小板活化和粘附。 CX3CR1在人主动脉平滑肌细胞上表达，CX3CR1 /载脂蛋白E双敲除小鼠的动脉粥样硬化病变面积和巨噬细胞募集明显减少。人群遗传学研究试图评估趋化因子在人类动脉粥样硬化中的重要性。当前，关于CCR2 / MCP-1和CCR5 / RANTES中的多态性与冠状动脉疾病之间的关联的证据相互矛盾。然而，有证据表明在人类和功能研究中，fractalkine受体多态性（CX3CR1-I249）与冠状动脉疾病之间存在关联。摘要：最近在动脉粥样硬化小鼠模型中进行的转基因和基因敲除研究突出了趋化因子及其受体在动脉粥样硬化中的重要性。关于趋化因子及其受体在人类研究中的作用的遗传证据仍在研究中。鉴定趋化因子多态性可以帮助确定在动脉粥样硬化疾病病理学中重要的途径，并可能提出新的治疗靶标。

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