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J Am Coll Cardiol, 2003; 41:1071-1077, doi:10.1016/S0735-1097(03)00088-3
© 2003 by the American College of Cardiology Foundation
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REVIEW ARTICLE

Atherothrombosis, inflammation, and diabetes

Giuseppe G. L. Biondi-Zoccai, MD*, Antonio Abbate, MD*, Giovanna Liuzzo, MD* and Luigi M. Biasucci, MD, FACC*,*

* Institute of Cardiology, Catholic University, Rome, Italy

Manuscript received August 15, 2002; revised manuscript received October 31, 2002, accepted November 19, 2002.

* Reprint requests and correspondence: Dr. Luigi M. Biasucci, Institute of Cardiology, Catholic University, Largo A. Gemelli 8, 00168 Rome, Italy.
lmbiasucci{at}virgilio.it

Diabetes represents a major cause of cardiovascular morbidity and mortality in developed countries, and atherothrombosis accounts for most deaths among diabetics. Recent evidence has reliably shown the relevant etiopathogenetic role of inflammation in atherothrombotic disease. This review summarizes and discusses the possible synergistic effects of diabetes and inflammation in promoting atherothrombosis and its complications, as well as potential avenues for diagnostic, preventive, and therapeutic benefits in the modulation of inflammatory mechanisms in diabetic atherothrombotic disease.

Abbreviations and Acronyms
  AGEP = advanced glycation end products
  CRP = C-reactive protein
  HDL = high-density lipoprotein
  ICAM-1 = intercellular adhesion molecule-1
  I-kappa-B = NF-kappa-B–inhibiting protein
  IL = interleukin
  LDL = low-density lipoprotein
  NF-kappa-B = nuclear factor-kappa-B
  NO = nitric oxide
  PAI-1 = plasminogen activator inhibitor-1
  PPAR = peroxisome proliferator-activated receptor
  TNF-alpha = tumor necrosis factor-alpha
  VCAM-1 = vascular cell adhesion molecule-1




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