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.
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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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