Published online before print February 24, 2005, doi: 10.1161/01.ATV.0000160340.72641.87
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© 2005 American Heart Association, Inc.
Brief Reviews |
Nuclear Factor 
B Signaling in Atherogenesis
From the Department of Molecular Genetics (M.P.J.d.W., M.H.H.), Cardiovascular Research Institute Maastricht, Maastricht University, The Netherlands; and the Department of Molecular Cell Biology and Immunology (E.K., G.K.), VU Medical Center, Amsterdam, The Netherlands.
Correspondence to Menno P.J. de Winther, PhD, Department of Molecular Genetics, Cardiovascular Research Institute Maastricht, UNS50/11, Universiteitssingel 50, 6229ER Maastricht, The Netherlands. E-mail dewinther{at}gen.unimaas.nl
Atherosclerosis is an inflammatory disease, characterized by the accumulation of macrophage-derived foam cells in the vessel wall and accompanied by the production of a wide range of chemokines, cytokines, and growth factors. These factors regulate the turnover and differentiation of immigrating and resident cells, eventually influencing plaque development. One of the key regulators of inflammation is the transcription factor nuclear factor 
B (NF-B), which, for a long time, has been regarded as a proatherogenic factor, mainly because of its regulation of many of the proinflammatory genes linked to atherosclerosis. NF-B may play an important role in guarding the delicate balance of the atherosclerotic process as a direct regulator of proinflammatory and anti-inflammatory genes and as a regulator of cell survival and proliferation. Here we address recent literature on the function of NF-B in inflammatory responses and its relation to atherosclerosis.
Atherosclerosis is an inflammatory disease, and a major transcription factor in inflammatory and immune responses is NF-B. We address recent literature on the function of NF-B in inflammatory responses and atherosclerosis and discuss its proatherogenic and antiatherogenic properties.
Key Words: atherosclerosis • signal transduction • immune system • macrophages
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