Key result
Elevated MCP-1 drives plaque vulnerability, monocyte infiltration, and restenosis across acute coronary syndromes.
Answers are grounded in this paper and cite their sources.
The designation of atherosclerosis as a chronic inflammatory process represents an exciting and logical paradigm shift for cardiologists. Monocyte chemoattractant protein-1 (MCP-1) plays an important role in the recruitment and activation of monocytes and thus in the development of atherosclerosis. Enhanced MCP-1 expression has been detected in macrophages, endothelial cells, and vascular smooth muscle cells in the atheromatous plaque. Activation of macrophages by MCP-1 also appears to be involved in the vulnerability of the plaque. Indeed, circulating MCP-1 levels are elevated in patients with acute myocardial infarction and in those with unstable angina, but not in patients with stable angina. Production of MCP-1 and macrophage accumulation are also observed after coronary angioplasty or grafting, indicating that MCP-1 expression may be related not only to instability of atheromatous plaques, but also to the formation of restenotic lesions. The development of therapeutic drugs for atherosclerosis targeted specially against MCP-1 may be useful in the prevention of plaque formation and future myocardial infarction.
No takes yet. Share an insight, caveat, or question.
Ikeda et al. (2002) conducted a review in Coronary artery disease and atherosclerosis. Monocyte chemoattractant protein-1 (MCP-1) was evaluated on Atherosclerosis development, plaque instability, and restenosis. Monocyte chemoattractant protein-1 (MCP-1) expression is elevated in acute myocardial infarction and unstable angina, driving monocyte recruitment, plaque vulnerability, and restenosis.
Synapse has enriched 10 related papers. Consider them for comparative context: