PMID- 15320854
OWN - NLM
STAT- MEDLINE
DCOM- 20041201
LR  - 20191026
IS  - 1570-1611 (Print)
IS  - 1570-1611 (Linking)
VI  - 1
IP  - 1
DP  - 2003 Mar
TI  - Inflammation and coronary artery disease.
PG  - 65-70
AB  - Several evidences, ranging from in vitro experiments, pathologic analysis and 
      epidemiologic studies, show that atherosclerosis is intrinsically an inflammatory 
      disease. The plasma concentrations of interleukin-6 (IL-6) and its hepatic 
      by-product, C-Reactive Protein (CRP), appear to reflect the intensity of occult 
      plaque inflammation and by inference may determine the vulnerability of plaque 
      rupture. The monocyte chemoattractant protein-1 (MCP-1) plays a crucial role in 
      initiating coronary artery disease by recruiting monocytes/macrophages to the 
      vessel wall. This leads to the formation of atherosclerotic lesions and also 
      increases the vulnerability of the plaque. Indeed, circulating IL-6 and MCP-1 
      levels are elevated in patients with acute myocardial infarction, and also in 
      patients with unstable angina, but not in those with stable angina. The plasma 
      IL-6 and MCP-1 concentrations are also increased after percutaneous coronary 
      intervention (PCI), and late restenosis is correlated with an increase in IL-6 or 
      MCP-1 concentrations after the procedure. This finding suggests that the 
      expression of IL-6 and MCP-1 may not only be related to the instability of 
      atheromatous plaques, but also to the formation of restenotic lesions after PCI. 
      The development of drugs specifically targeted against IL-6 and MCP-1 may be 
      useful in the prevention of plaque formation, myocardial infarction and 
      restenosis.
FAU - Ikeda, Uichi
AU  - Ikeda U
AD  - Division of Cardiovascular Medicine, Jichi Medical School, Tochigi, Japan. 
      uikeda@jichi.ac.jp
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United Arab Emirates
TA  - Curr Vasc Pharmacol
JT  - Current vascular pharmacology
JID - 101157208
RN  - 0 (Chemokine CCL2)
RN  - 0 (Interleukin-6)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/antagonists & inhibitors/immunology
MH  - Coronary Artery Disease/drug therapy/*immunology
MH  - Humans
MH  - Inflammation/*immunology
MH  - Interleukin-6/physiology
RF  - 78
EDAT- 2004/08/24 05:00
MHDA- 2004/12/16 09:00
CRDT- 2004/08/24 05:00
PHST- 2004/08/24 05:00 [pubmed]
PHST- 2004/12/16 09:00 [medline]
PHST- 2004/08/24 05:00 [entrez]
AID - 10.2174/1570161033386727 [doi]
PST - ppublish
SO  - Curr Vasc Pharmacol. 2003 Mar;1(1):65-70. doi: 10.2174/1570161033386727.