Nuclear factor kappaB: a potential therapeutic target in atherosclerosis and thrombosis. Export

@article{citeulike:276734, abstract = {Cardiovascular diseases are the leading cause of morbidity and mortality in Western countries. Atherosclerosis, the background for many cardiovascular diseases, is characterized by the accumulation of lipid and fibrotic entities in large arteries and bears many similarities with chronic inflammatory diseases such as rheumatoid arthritis. Common features include extravasation of blood-derived leukocytes, as well as production of cytokines, chemokines and matrix-degrading enzymes. There are also many shared signaling pathways, including activation of the nuclear factor kappaB (NFkappaB) cascade. In the context of atherosclerosis, there are a range of candidate stimuli which can activate NFkappaB, including traditional risk factors, infectious agents, cytokines and cell-cell contact. Many inflammatory genes relevant to the pathogenesis of atherosclerosis are regulated by NFkappaB, the activated form of which is present in atherosclerotic plaques. Thus, it is essential to understand the role of this important signaling cascade in atherosclerosis, in a quest for more specific therapeutic targets.}, address = {Faculty of Medicine, Kennedy Institute of Rheumatology, Imperial College, Arthritis Research Campaign Building, 1, Aspenlea Road, London W6 8LH, UK.}, author = {Monaco, C. and Paleolog, E.}, citeulike-article-id = {276734}, citeulike-linkout-0 = {http://dx.doi.org/10.1016/j.cardiores.2003.11.038}, citeulike-linkout-1 = {http://view.ncbi.nlm.nih.gov/pubmed/14985064}, citeulike-linkout-2 = {http://www.hubmed.org/display.cgi?uids=14985064}, day = {1}, doi = {10.1016/j.cardiores.2003.11.038}, issn = {0008-6363}, journal = {Cardiovasc Res}, keywords = {atherosclerosis, fattyacids, ffa, nfkb}, month = {March}, number = {4}, pages = {671--682}, posted-at = {2005-08-08 11:26:40}, priority = {2}, title = {Nuclear factor kappaB: a potential therapeutic target in atherosclerosis and thrombosis.}, url = {http://dx.doi.org/10.1016/j.cardiores.2003.11.038}, volume = {61}, year = {2004} }

TY - JOUR ID - citeulike:276734 L3 - citeulike-article-id:276734 N2 - Cardiovascular diseases are the leading cause of morbidity and mortality in Western countries. Atherosclerosis, the background for many cardiovascular diseases, is characterized by the accumulation of lipid and fibrotic entities in large arteries and bears many similarities with chronic inflammatory diseases such as rheumatoid arthritis. Common features include extravasation of blood-derived leukocytes, as well as production of cytokines, chemokines and matrix-degrading enzymes. There are also many shared signaling pathways, including activation of the nuclear factor kappaB (NFkappaB) cascade. In the context of atherosclerosis, there are a range of candidate stimuli which can activate NFkappaB, including traditional risk factors, infectious agents, cytokines and cell-cell contact. Many inflammatory genes relevant to the pathogenesis of atherosclerosis are regulated by NFkappaB, the activated form of which is present in atherosclerotic plaques. Thus, it is essential to understand the role of this important signaling cascade in atherosclerosis, in a quest for more specific therapeutic targets. IS - 4 JF - Cardiovasc Res SN - 0008-6363 AD - Faculty of Medicine, Kennedy Institute of Rheumatology, Imperial College, Arthritis Research Campaign Building, 1, Aspenlea Road, London W6 8LH, UK. EP - 682 TI - Nuclear factor kappaB: a potential therapeutic target in atherosclerosis and thrombosis. VL - 61 SP - 671 KW - atherosclerosis KW - fattyacids KW - ffa KW - nfkb AU - Monaco, C AU - Paleolog, E PY - 2004/03/01/ UR - http://dx.doi.org/10.1016/j.cardiores.2003.11.038 ER -