Disrupting atherosclerosis Export

@article{citeulike:4670529, abstract = {A team of German and U.S. researchers has designed a peptide that decreases atherosclerotic lesions in mice by disrupting interactions between two platelet-derived chemokines.1 The findings have led to the formation of Carolus Therapeutics Inc., which is developing the peptide for cardiovascular and inflammatory disorders. Atherosclerotic lesions and plaques occur as a result of a series of inflammatory processes on the walls of blood vessels.2 In particular, adhesion of circulating leukocytes and platelets to inflamed arterial endothelial cells increases vessel permeability to plasma lipid components like plaque-forming low-density lipoprotein (LDL). Over time, plaques accumulate, causing a narrowing of the vessel lumen. Occasionally, plaques rupture and release debris, triggering the formation of a thrombus, which can obstruct blood flow and result in myocardial infarction or stroke (see Figure1, "Targeting chemokines in cardiovascular disease").}, author = {Fulmer, Tim}, citeulike-article-id = {4670529}, citeulike-linkout-0 = {http://dx.doi.org/10.1038/scibx.2009.79}, citeulike-linkout-1 = {http://www.nature.com/scibx/journal/v2/n3/pdf/scibx.2009.79.pdf}, day = {22}, doi = {10.1038/scibx.2009.79}, issn = {1945-3477}, journal = {Science-Business eXchange}, keywords = {angiogenesis, atherosclerosis, chemokines}, month = {January}, number = {3}, pages = {1--3}, posted-at = {2009-05-28 22:49:37}, priority = {2}, title = {Disrupting atherosclerosis}, url = {http://dx.doi.org/10.1038/scibx.2009.79}, volume = {2}, year = {2009} }

TY - JOUR ID - citeulike:4670529 L3 - citeulike-article-id:4670529 N2 - A team of German and U.S. researchers has designed a peptide that decreases atherosclerotic lesions in mice by disrupting interactions between two platelet-derived chemokines.1 The findings have led to the formation of Carolus Therapeutics Inc., which is developing the peptide for cardiovascular and inflammatory disorders. Atherosclerotic lesions and plaques occur as a result of a series of inflammatory processes on the walls of blood vessels.2 In particular, adhesion of circulating leukocytes and platelets to inflamed arterial endothelial cells increases vessel permeability to plasma lipid components like plaque-forming low-density lipoprotein (LDL). Over time, plaques accumulate, causing a narrowing of the vessel lumen. Occasionally, plaques rupture and release debris, triggering the formation of a thrombus, which can obstruct blood flow and result in myocardial infarction or stroke (see Figure1, "Targeting chemokines in cardiovascular disease"). IS - 3 JF - Science-Business eXchange SN - 1945-3477 EP - 3 TI - Disrupting atherosclerosis VL - 2 SP - 1 KW - angiogenesis KW - atherosclerosis KW - chemokines AU - Fulmer, Tim PY - 2009/01/22/ UR - http://dx.doi.org/10.1038/scibx.2009.79 ER -