We are analyzing https://link.springer.com/article/10.1007/s00395-005-0511-6.

Title:
Inflammatory mediators in atherosclerotic vascular disease | Basic Research in Cardiology
Description:
An impressive body of work has established the current paradigm of atherosclerosis as an inflammatory process that promotes lesion development and progression. Early atheroma formation is characterized by leukocyte recruitment and expression of inflammatory mediators which is confounded in the context of hyperlipidemia. Evidence for an involvement of both innate and adaptive immunity in lesion formation has emerged, supporting a causal relation between the balance of pro- and anti–inflammatory cytokines and atherogenesis. The function of chemokines in distinct steps during mononuclear cell recruitment to vascular lesions has been studied in genetically deficient mice and other suitable models, and displays a high degree of specialization and cooperation. The contribution of platelet chemokines deposited on endothelium to monocyte arrest, differences in the presentation and involvement of chemokines between native and neointimal lesion formation, and related functions of macrophage migration inhibitory factor, a cytokine with striking structural homology to chemokines are of note. A novel role of chemokines in the recruitment of vascular progenitors during neointimal hyperplasia and in the recovery of endothelial denudation underscores their relevance for atherosclerotic vascular disease. The functional diversity of chemokines in vascular inflammation may potentially allow the selective therapeutic targeting of different atherosclerotic conditions.
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Keywords {🔍}

google, scholar, atherosclerosis, mice, chemokine, weber, chemokines, atherosclerotic, article, monocyte, human, vascular, factor, receptor, biol, cells, circulation, ccr, res, thromb, vasc, expression, role, arterioscler, formation, cxcr, protein, chemoattractant, circ, nature, cas, pubmed, cell, clin, invest, injury, recruitment, atherogenesis, endothelium, macrophage, migration, inhibitory, apolipoprotein, libby, fractalkine, neointimal, receptors, interleukin, cxc, tumor,

Topics {✒️}

stromal cell-derived factor-1_ stromal cell-derived factor-1a month download article/chapter chemokine stromal-derived factor-1 ifn-gamma potentiates atherosclerosis mm-ldl-stimulated endothelium cell-surface scavenger receptor interferon-γ-regulated chemokine ldl receptor-deficient mice article basic research apolipoprotein e-deficient mice shear-resistant adhesion- induction smooth muscle cells macrophage-derived chemokine monocyte chemoattractant protein-1 macrophage-derived mediator interferon–γ il anti–inflammatory cytokines full article pdf stem cell mobilization privacy choices/manage cookies apoe-deficient mice selective therapeutic targeting modulate receptor binding activated platelets triggers membrane- bound chemokine cc chemokine i-309 cd18 inhibits experimental enhances plaque formation glomerular monocyte recruitment genetically deficient mice macrophage foam cells mononuclear cell recruitment platelet factor 4 macrophage-rich areas platelet chemokines deposited triggers monocyte arrest chemokine receptor cxcr4 garcia-zepeda ea tgf-beta signaling apoe knockout mice scavenger receptor expressed endothelial denudation underscores atherosclerotic vascular disease atherosclerotic arteries suggests interleukin-1 receptor antagonist inhibitory potential depends vascular dendritic cells related subjects differential chemokine immobilization

Schema {🗺️}

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         description:An impressive body of work has established the current paradigm of atherosclerosis as an inflammatory process that promotes lesion development and progression. Early atheroma formation is characterized by leukocyte recruitment and expression of inflammatory mediators which is confounded in the context of hyperlipidemia. Evidence for an involvement of both innate and adaptive immunity in lesion formation has emerged, supporting a causal relation between the balance of pro- and anti–inflammatory cytokines and atherogenesis. The function of chemokines in distinct steps during mononuclear cell recruitment to vascular lesions has been studied in genetically deficient mice and other suitable models, and displays a high degree of specialization and cooperation. The contribution of platelet chemokines deposited on endothelium to monocyte arrest, differences in the presentation and involvement of chemokines between native and neointimal lesion formation, and related functions of macrophage migration inhibitory factor, a cytokine with striking structural homology to chemokines are of note. A novel role of chemokines in the recruitment of vascular progenitors during neointimal hyperplasia and in the recovery of endothelial denudation underscores their relevance for atherosclerotic vascular disease. The functional diversity of chemokines in vascular inflammation may potentially allow the selective therapeutic targeting of different atherosclerotic conditions.
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