File:PMC4577534 109 2015 1317 Fig1 HTML.png

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Attribution 4.0 International (CC BY 4.0)

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Author:van der Vorst EP, Döring Y, Weber C, Institute for Cardiovascular Prevention, Ludwig-Maximilians-University Munich (Openi/National Library of Medicine) Source:https://openi.nlm.nih.gov/detailedresult?img=PMC4577534_109_2015_1317_Fig1_HTML&query=Leukocyte%20adhesion%20molecule%20deficiency&it=xg&req=4&npos=11 Description:Fig1: Role of chemokines in atherosclerosis. After endothelial cell damage, LDL will migrate into the intima, where it will undergo oxidation (1). Modified LDL will subsequently be taken up by macrophages, forming foam cells (2). Lysophosphatidic acid, a component of LDL, induces endothelial CXCL1 secretion to recruit monocytes via CXCR2. CCR1 and CCR5 are crucial chemokine receptors for leukocyte recruitment (3). Recruited leukocytes will adhere to the vessel wall, using VCAM-1-VLA4 and ICAM1-LFA1 interactions (4). Continuous accumulation of lipids and debris will eventually result in apoptosis of lesional macrophages. CX3CR1 is important for monocyte survival, by protecting them from apoptosis (5). Upon lesion progression, a fibrous cap is formed to protect the lumen from the necrotic core. This cap consists of collagen and elastin, produced by SMCs. CXCL10 inhibits SMC proliferation, thereby influencing plaque stability (6). CCR7 can mediate monocyte/macrophage egress from lesions (7). Upon lesion rupture, platelets adhere to the site of injury, and a thrombus is formed (8). CXCL12, CCL17, and CCL22 play an important role in platelet activation and aggrevation. ICAM1 intercellular adhesion molecule 1, JAM junctional adhesion molecule, LDL low-density lipoproteins, LFA1 lymphocyte function-associated antigen 1, MMP matrix metalloproteases, SMCs smooth muscle cells, VCAM1 vascular cell adhesion molecule 1, VLA4 very late antigen 4