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
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Figure 1 The pathogenetic mechanisms involved in the initiation of subclinical atherosclerosis and progression to atherosclerotic clinical events in diabetic patients include infection, inflammation, hyperglycemia, insulin resistance, dyslipidemia, and thrombosis. AGE = advanced glycation end products; CRP = C-reactive protein; HDL = high-density lipoprotein; HTN = hypertension; IL-6 = interleukin-6; LDL = low-density lipoprotein; PAI-1 = plasminogen activator inhibitor-1; SAA = serum amyloid A protein; TF = tissue factor; TG = triglycerides; tPA = tissue-type plasminogen activator.
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Figure 2 Reciprocal interplay between inflammation and diabetes mellitus in the pathogenesis of atherothrombosis, with emphasis on both the role of inflammation in the development of overt diabetes mellitus and the proinflammatory action of hyperglycemia and insulin resistance. Potential or established modulating agents are shown by dashed arrows. ACEi = angiotensin-converting enzyme inhibitors; ARB = angiotensin receptor blockers; PPAR = peroxisome proliferator-activated receptor.
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