Are endothelial cells involved in atherosclerosis?
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Under a Creative Commons license Open access • Intimal neovascularization in
plaque growth and destabilization. Role of classical and specific angiogenic factors in atherosclerotic angiogenesis. Inflammation and oxidative stress promote angiogenesis and plaque destabilization. Angiogenesis promote intraplaque hemorrhages, afflux of blood cells and lipids. Anti-angiogenic therapy for atherosclerotic angiogenesis. AbstractAtherosclerosis is a multifocal alteration of the vascular wall of medium and large arteries characterized by a local accumulation of cholesterol and non-resolving inflammation. Atherothrombotic complications are the leading cause of disability and mortality in western countries. Neovascularization in atherosclerotic lesions plays a major role in plaque growth and instability. The angiogenic process is mediated by classical angiogenic factors and by additional factors specific to atherosclerotic angiogenesis. In addition to its role in plaque progression, neovascularization may take part in plaque destabilization and thromboembolic events. Anti-angiogenic agents are effective to reduce atherosclerosis progression in various animal models. However, clinical trials with anti-angiogenic drugs, mainly anti-VEGF/VEGFR, used in anti-cancer therapy show cardiovascular adverse effects, and require additional investigations. AbbreviationsADMA assymetric methylarginine ABCG1 ATP-binding cassette sub-family G member 1 AIBP ApoA-I binding protein ApoE−/− mice homozygous ApoE-deficient mice ARNT aryl hydrocarbon nuclear translocator CPT1A carnitine palmityl transferase EGF epidermal growth factor eNOS endothelial nitric oxide synthase ERK extracellular signal-regulated kinase FGF basic fibroblast growth factor; HDL high density lipopoprotein HIF Hypoxia inducible factor HSP heparan sulfate proteoglycans Flt-1 fms-like tyrosine kinase-1 HUVEC human umbilical vein endothelial cell ICAM-1 InterCellular Adhesion Molecule-1 iNOS inducible nitric oxide synthase LDLs low density lipoproteins MAPK mitogen activated protein kinase MMP matrix metalloproteinase NADPH H+, nicotinamide adenine dinucleotide phosphate nNOS neuronal nitric oxide synthase NF-kB nuclear factor kappaB PAI-1 plasminogen activator inhibitor 1 nSMase2 neutral sphingomyelinase-2 PDGF platelet-derived growth factor PI3K phosphoinositide 3 kinase PUFA polyunsaturated fatty acid PPAR peroxisome proliferator activated receptor RCT reverse cholesterol transport ROCK Rho associated protein kinase RTKs receptor tyrosine kinase ROS reactive oxygen species S1P sphingosine 1-phosphate Spns2 S1P carry spinster homolog 2 SRC Sarcoma tyrosine kinase TGF-β transforming growth factor-β TIMPs Tissue Inhibitor of Metalloproteinases VCAM-1 Vascular Cell Adhesion Molecule-1 VEGF vascular endothelial growth factor KeywordsNeovascularization Angiogenesis VEGF Atherosclerosis Hypercholesterolemia Cited by (0)© 2017 The Authors. Published by Elsevier B.V. What cells are involved in atherosclerosis?Atherosclerosis is a multiphase process which is characterized with the activation of endothelial cells with the expression of adhesion molecules and monocytes/macrophages, and the transmigration of DCs, T cells and some B-cells into the intima, and also the transfer of modulated types of LDL to matrix components.
What happens to endothelial cells in atherosclerosis?Endothelial cells (ECs) line all blood vessels and are critical mediators of inflammatory responses. In the setting of atherosclerosis, ECs become chronically activated through a combination of turbulent blood flow, lipid accumulation in the vessel wall and exposure to inflammatory mediators (for example, IL-1β)1.
What are endothelial cells responsible for?Endothelial cells form a single cell layer that lines all blood vessels and regulates exchanges between the bloodstream and the surrounding tissues. Signals from endothelial cells organize the growth and development of connective tissue cells that form the surrounding layers of the blood-vessel wall.
What happens to cells during atherosclerosis?Abstract— During the development of an atherosclerotic plaque, mononuclear leukocytes infiltrate the artery wall through vascular endothelial cells (ECs). At the same time, arterial smooth muscle cells (SMCs) change from the physiological contractile phenotype to the secretory phenotype and migrate into the plaque.
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