Cytokines in atherosclerosis: Key players in all stages of disease and promising therapeutic targets. Issue 6 (December 2015)

• Record Type: Journal Article
• Authors: Ramji, Dipak P.; Davies, Thomas S.
• Is Part Of: Cytokine & growth factor reviews. Volume 26:Issue 6(2015)
• Page Start: 673
• Page End: 685
• Publication Date: 2015-12
• Subjects: Atherosclerosis -- Cytokines -- Chemokines -- Inflammation -- Therapeutic avenues; ABC ATP-binding cassette -- ACAT-1 acyl-CoA acyl transferase-1 -- ADRP adipocyte differentiation related protein -- Apo apolipoprotein -- BMT bone marrow transplantation -- CANTOS Canakinumab Anti-inflammatory Thrombosis Outcomes Study -- CIRT Cardiovascular Inflammation Reduction Trial -- CCR2 CC-chemokine receptor-2 -- CR chemokine receptor -- CVD cardiovascular disease -- CSF colony-stimulating factor -- DCs dendritic cells -- ECs endothelial cells -- ECM extracellular matrix -- eNOS endothelial nitric oxide synthase -- ER endoplasmic reticulum -- ERK extracellular signal-regulated kinase -- Fn14 fibroblast growth factor-inducible 14 -- G-CSF granulocyte colony-stimulating factor -- GDF-15 growth differentiation factor-15 -- GM-CSF granulocyte macrophage colony-stimulating factor -- ICAM-1 intercellular adhesion molecule-1 -- IFN interferon -- IL interleukin -- IL-18BP IL-18 binding protein -- IL-1RA IL-1 receptor antagonist -- LDL low-density lipoprotein -- LDLr low-density lipoprotein receptor -- LFA1 lymphocyte function-associated antigen 1 -- LIGHT homologous to lymphotoxin, exhibits inducible expression, and competes with HSV glycoprotein D for herpes virus entry mediator, a receptor expressed by T lymphocytes -- M-CSF macrophage-colony stimulating factor -- MHC major histocompatibility complex -- MIF macrophage migration inhibitory factor -- miRNA micro RNA -- mmLDL minimally modified LDL -- MMP matrix metalloproteinase -- LXR liver X receptors -- NK natural killer -- NOD nucleotide-binding oligomerization domain -- NLR NOD-like receptor -- NLRP3 NLR family, pyrin domain containing 3 -- NPC Niemann-Pick disease, type C -- OxLDL oxidized LDL -- PAI plasminogen activator inhibitor -- PECAM-1 platelet endothelial cell adhesion molecule-1 -- PRR pattern recognition receptor -- RCT reverse cholesterol transport -- ROS reactive oxygen species -- SMCs smooth muscle cells -- SOCS suppressor of cytokine signaling -- SR scavenger receptor -- SREBP sterol response element binding protein -- SR-PSOX SR that binds phosphatidyl serine and oxidized lipoprotein -- STAT1 signal transducer and activator of transcription-1 -- TF tissue factor -- TGF transforming growth factor -- Th T-helper -- TIMP tissue inhibitor of metalloproteinases -- TNF tumor necrosis factor -- TL1A TNF-like protein 1A -- TNFSF12 TNF superfamily member 12 -- TLR Toll-like receptor -- TRAIL TNF-related apoptosis-inducing ligand -- Tregs regulatory T cells -- TWEAK TNF-related weak inducer of apoptosis -- VCAM-1 vascular cell adhesion molecule-1 -- VLA4 very late antigen 4 -- wt wild type; Cytokines -- Periodicals; 571.84
• DOI: 10.1016/j.cytogfr.2015.04.003
• Languages: English
• ISSNs: 1359-6101

Abstract

Abstract: Atherosclerosis, a chronic inflammatory disorder of the arteries, is responsible for most deaths in westernized societies with numbers increasing at a marked rate in developing countries. The disease is initiated by the activation of the endothelium by various risk factors leading to chemokine-mediated recruitment of immune cells. The uptake of modified lipoproteins by macrophages along with defective cholesterol efflux gives rise to foam cells associated with the fatty streak in the early phase of the disease. As the disease progresses, complex fibrotic plaques are produced as a result of lysis of foam cells, migration and proliferation of vascular smooth muscle cells and continued inflammatory response. Such plaques are stabilized by the extracellular matrix produced by smooth muscle cells and destabilized by matrix metalloproteinase from macrophages. Rupture of unstable plaques and subsequent thrombosis leads to clinical complications such as myocardial infarction. Cytokines are involved in all stages of atherosclerosis and have a profound influence on the pathogenesis of this disease. This review will describe our current understanding of the roles of different cytokines in atherosclerosis together with therapeutic approaches aimed at manipulating their actions.