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(Circulation Research. 2008;103:e116.)
© 2008 American Heart Association, Inc.

Letter to the Editor

Diabetes-Accelerated Atherosclerosis and Inflammation

Jenny E. Kanter, Michelle M. Averill, Renee C. LeBoeuf, Karin E. Bornfeldt

Departments of Pathology and Medicine, Diabetes and Obesity Center of Excellence, University of Washington School of Medicine, Seattle, WA, E-mail bornf@u.washington.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

We read with interest the Letter to the Editor by Marfella et al¹ in response to our review article on the role of glucose and lipids in diabetes-accelerated atherosclerosis.² Marfella et al¹ point out that inflammation is likely to play important roles in diabetes-associated cardiovascular events. Indeed, in our review article,² we highlighted recent data suggesting that both elevated glucose and lipids contribute to increased inflammation. There is increasing evidence that type 1 and type 2 diabetes are associated with an enhanced inflammatory state and that inflammatory cells contribute to atherosclerotic lesion initiation and lesion disruption.

Accordingly, type 1 diabetes can cause increases in several circulating inflammatory markers, such as C-reactive protein, soluble intercellular adhesion molecule, CD40 ligand, interleukin (IL)-6, and S100A9.^3–5 In addition, type 1 diabetes can promote a proinflammatory state in monocytes, associated with elevated IL-6, IL-8, IL-1, and CCL2.^3–4,6 Given the inflammatory basis of atherosclerosis, these findings suggest that type 1 diabetes may accelerate atherosclerosis, in part, by stimulating inflammatory monocytes and/or systemic inflammatory mediators. Indeed, intense insulin therapy results in a coordinated reduction in certain circulating inflammatory markers and reduced risk for cardiovascular complications.⁷ Furthermore, type 1 diabetes might stimulate accumulation of highly inflammatory macrophage populations in atherosclerotic lesions. In a mouse model of type 1 diabetes–accelerated lesion disruption, S100A9 is upregulated in monocytes/macrophages.⁸ S100A9 has recently been shown to be a marker of acute coronary syndromes in humans, further supporting an augmented inflammatory state contributing to cardiovascular disease in type 1 . . . [Full Text of this Article]