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(Circulation Research. 2007;100:e84.)
© 2007 American Heart Association, Inc.

Letters to the Editor

Diabetes, Ubiquitin Proteasome System and Atherosclerotic Plaque Rupture

Raffaele Marfella, Clara Di Filippo, Michele D’Amico, Giuseppe Paolisso

Department of Geriatrics and Metabolic Diseases, Cardiovascular Research Center, Second University of Naples, Italy

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 review of Kanter and coworkers about the role of glucose and lipids on atherosclerotic lesion initiation or progression to advanced plaques.¹ He pointed out that hyperglycemia alone appears insufficient to accelerate atherosclerosis, at least in various animal models. He adds that little is still known about the role of diabetes in accelerating cardiovascular events merely by inducing an accelerated progression of atherosclerotic lesions. Finally, he concludes that studies on advanced lesions will be necessary to further our knowledge on the cellular and molecular mechanisms whereby diabetes leads to cardiovascular events. This gap in knowledge, reducing the role of the hyperglycemia on atherosclerosis progression toward plaque rupture, may limit the therapeutic strategy to reduce the impact of diabetes on cardiovascular events. In recent years, it has been firmly established that inflammation contributes to plaque rupture and cardiovascular events.² Several inflammatory markers have been identified in atherosclerotic lesions. Among them are cytokines and growth factors, which are released by activated macrophages that, together with T cells, are major cellular components in atherosclerotic lesions.³ However, the inflammatory burden linked to diabetes may contribute to plaque rupture and cardiovascular disease (CVD).⁴ A thin fibrous cap and a large lipid core in association with inflammatory cell infiltration and necrotic areas, apoptosis of vascular cells (VSMC), decrease in collagen production, and increase in collagen degradation are key characteristics of the unstable atheroma.³ In atherectomy specimens, the cell-rich and necrotic areas are increased in de novo lesions in persons . . . [Full Text of this Article]

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				J. E. Kanter, M. M. Averill, R. C. LeBoeuf, and K. E. Bornfeldt Diabetes-Accelerated Atherosclerosis and Inflammation Circ. Res., October 10, 2008; 103(8): e116 - e117. [Full Text] [PDF]