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REVIEW ARTICLE

Atherothrombosis, inflammation, and diabetes

^* 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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