{"title":"JAM-A：动脉粥样硬化中的粘附受体和信号调节因子。","authors":"Mariel F Schwietzer, Klaus Ebnet","doi":"10.1007/s11883-025-01322-x","DOIUrl":null,"url":null,"abstract":"<p><strong>Purpose of review: </strong>Cell-cell adhesion between leukocytes, platelets and endothelial cells plays a critical role in vascular inflammation and thrombus formation. This review aims at providing a comprehensive picture of the contribution of the immunoglobulin superfamily (IgSF) cell adhesion receptor Junctional Adhesion Molecule-A (JAM-A) to the process of atherosclerosis.</p><p><strong>Recent findings: </strong>Proinflammatory and proatherogenic stimulation of endothelial cells results in redistribution of JAM-A from cell-cell junctions to the apical surface to promote monocyte adhesion and transmigration. Agonist-stimulation of platelets results in elevated surface levels of JAM-A concomitant with enhanced release of soluble JAM-A (sJAM-A). sJAM-A promotes platelet aggregation, thrombus formation, and platelet-monocyte aggregate formation. Elevated levels of sJAM-A correlate with recurrent myocardial infarction. JAM-A is expressed by several cell types implicated in atherogenesis, notably endothelial cells, platelets, and leukocytes. Proinflammatory and proatherogenic stimuli induce a redistribution of JAM-A within endothelial cells. Stimulated platelets release sJAM-A into the circulation. This review illustrates the role of JAM-A in atherogenesis and elaborates the underlying mechanisms.</p>","PeriodicalId":10875,"journal":{"name":"Current Atherosclerosis Reports","volume":"27 1","pages":"75"},"PeriodicalIF":5.2000,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12307491/pdf/","citationCount":"0","resultStr":"{\"title\":\"JAM-A: Adhesion Receptor and Signaling Regulator in Atherosclerosis.\",\"authors\":\"Mariel F Schwietzer, Klaus Ebnet\",\"doi\":\"10.1007/s11883-025-01322-x\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Purpose of review: </strong>Cell-cell adhesion between leukocytes, platelets and endothelial cells plays a critical role in vascular inflammation and thrombus formation. This review aims at providing a comprehensive picture of the contribution of the immunoglobulin superfamily (IgSF) cell adhesion receptor Junctional Adhesion Molecule-A (JAM-A) to the process of atherosclerosis.</p><p><strong>Recent findings: </strong>Proinflammatory and proatherogenic stimulation of endothelial cells results in redistribution of JAM-A from cell-cell junctions to the apical surface to promote monocyte adhesion and transmigration. Agonist-stimulation of platelets results in elevated surface levels of JAM-A concomitant with enhanced release of soluble JAM-A (sJAM-A). sJAM-A promotes platelet aggregation, thrombus formation, and platelet-monocyte aggregate formation. Elevated levels of sJAM-A correlate with recurrent myocardial infarction. JAM-A is expressed by several cell types implicated in atherogenesis, notably endothelial cells, platelets, and leukocytes. Proinflammatory and proatherogenic stimuli induce a redistribution of JAM-A within endothelial cells. Stimulated platelets release sJAM-A into the circulation. This review illustrates the role of JAM-A in atherogenesis and elaborates the underlying mechanisms.</p>\",\"PeriodicalId\":10875,\"journal\":{\"name\":\"Current Atherosclerosis Reports\",\"volume\":\"27 1\",\"pages\":\"75\"},\"PeriodicalIF\":5.2000,\"publicationDate\":\"2025-07-29\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12307491/pdf/\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Current Atherosclerosis Reports\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1007/s11883-025-01322-x\",\"RegionNum\":2,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"PERIPHERAL VASCULAR DISEASE\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current Atherosclerosis Reports","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s11883-025-01322-x","RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"PERIPHERAL VASCULAR DISEASE","Score":null,"Total":0}
引用次数: 0
摘要
白细胞、血小板和内皮细胞之间的细胞粘附在血管炎症和血栓形成中起着至关重要的作用。本文旨在全面介绍免疫球蛋白超家族（IgSF）细胞粘附受体连接粘附分子- a （JAM-A）在动脉粥样硬化过程中的作用。最近发现：内皮细胞的促炎和促动脉粥样硬化刺激导致JAM-A从细胞-细胞连接处重新分布到根尖表面，促进单核细胞粘附和转运。激动剂刺激血小板导致表面JAM-A水平升高，同时可溶性JAM-A （sJAM-A）释放增强。sJAM-A促进血小板聚集、血栓形成和血小板单核细胞聚集形成。高水平的sJAM-A与复发性心肌梗死相关。JAM-A在几种与动脉粥样硬化有关的细胞类型中表达，特别是内皮细胞、血小板和白细胞。促炎和致动脉粥样硬化刺激诱导内皮细胞内JAM-A的重新分配。受刺激的血小板将sJAM-A释放到血液循环中。本文综述了JAM-A在动脉粥样硬化中的作用，并阐述了其潜在的机制。
JAM-A: Adhesion Receptor and Signaling Regulator in Atherosclerosis.
Purpose of review: Cell-cell adhesion between leukocytes, platelets and endothelial cells plays a critical role in vascular inflammation and thrombus formation. This review aims at providing a comprehensive picture of the contribution of the immunoglobulin superfamily (IgSF) cell adhesion receptor Junctional Adhesion Molecule-A (JAM-A) to the process of atherosclerosis.
Recent findings: Proinflammatory and proatherogenic stimulation of endothelial cells results in redistribution of JAM-A from cell-cell junctions to the apical surface to promote monocyte adhesion and transmigration. Agonist-stimulation of platelets results in elevated surface levels of JAM-A concomitant with enhanced release of soluble JAM-A (sJAM-A). sJAM-A promotes platelet aggregation, thrombus formation, and platelet-monocyte aggregate formation. Elevated levels of sJAM-A correlate with recurrent myocardial infarction. JAM-A is expressed by several cell types implicated in atherogenesis, notably endothelial cells, platelets, and leukocytes. Proinflammatory and proatherogenic stimuli induce a redistribution of JAM-A within endothelial cells. Stimulated platelets release sJAM-A into the circulation. This review illustrates the role of JAM-A in atherogenesis and elaborates the underlying mechanisms.
期刊介绍：
The aim of this journal is to systematically provide expert views on current basic science and clinical advances in the field of atherosclerosis and highlight the most important developments likely to transform the field of cardiovascular prevention, diagnosis, and treatment.
We accomplish this aim by appointing major authorities to serve as Section Editors who select leading experts from around the world to provide definitive reviews on key topics and papers published in the past year. We also provide supplementary reviews and commentaries from well-known figures in the field. An Editorial Board of internationally diverse members suggests topics of special interest to their country/region and ensures that topics are current and include emerging research.
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号
