Nuclear Factor B Signaling in Atherogenesis

Abstract—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. (Arterioscler Thromb Vasc Biol. 2005;25:904-914.) Key Words: atherosclerosis signal transduction immune system macrophages Atherosclerosis is a slowly progressing inflammatorydisease of the medium- and large-sized arteries,1 result-ing in the formation of fatty and fibrous lesions in the vessel wall. It is the major cause of cardiovascular diseases and is responsible for a large proportion of mortality in our Western society.