Independent Roles of Monocyte Chemoattractant Protein-1, Regulated on Activation, Normal T-Cell Expressed and Secreted and Fractalkine in the Vulnerability of Coronary Atherosclerotic Plaques

Effect of Folic Acid Supplementation on Levels of Circulating Monocyte Chemoattractant Protein-1 and the Presence of Intravascular Ultrasound Derived Virtual Histology Thin-Cap Fibroatheromas in Patients with Stable Angina Pectoris

“…Monocyte infiltration is a prerequisite for the development of atherosclerotic lesions, and MCP-1 plays an essential role [11-13]. MCP-1 levels and mRNA expression have recently been associated with acute coronary syndrome and plaque rupture [42]. We found that MCP-1 was correlated to VH-TCFA lesions and independently predicted MI, and 25% of patients in our study with VH-TCFA experienced a coronary event within 2 years.…”

Chemokines and atherosclerosis: focus on the CX3CL1/CX3CR1 pathway

“…Li et al assessed the concentrations and mRNA expression levels of CCL2, CCL5, and CX3CL1 in 60 patients with acute myocardial infarction, 60 patients with unstable angina pectoris, 60 patients with stable angina pectoris and 40 patients without coronary heart disease. The authors observed significantly higher chemokine levels in unstable coronary artery disease patients compared to stable coronary artery disease patients [37] . Similarly, Damås et al assessed plasma levels of CX3CL1 and CX3CR1 expression in peripheral blood mononuclear cells of various coronary artery disease populations and concluded that the plasma levels of CX3CL1 are greatly increased in coronary artery disease, particularly in unstable angina with parallel increase of CX3CR1 expression in peripheral blood mononuclear cells.…”

Changes in fractalkine in patients with ST-elevation myocardial infarction

“…Combadière et al [7] found that the CX3CR1-CX3CL1 pathway plays a direct and major role in the development of macrophage-rich atherosclerotic lesions and that CX3CR1/apolipoprotein E double knockout mice show decreased atherosclerotic lesion formation. Recently, our [10,11,15] and several other studies [16,17] detected increases in sFKN and CX3CR1-expressing monocytes significantly related to plaque rupture in unstable angina pectoris (UAP) patients. To date, there have been limited reports on FKN in AMI in humans.…”