In addition to promoting atherogenesis, diabetes conveys plaque instability.21 It has been shown that atherosclerotic lesions in diabetic patients have fewer vascular smooth muscle cells compared with those of controls. As the source of collagen, vascular smooth muscle cells strengthen the atheroma, making it less likely to rupture and cause thrombosis. In addition, diabetic endothelial cells may produce an excess of cytokines that decrease the de novo synthesis of collagen by vascular smooth muscle cells. Finally, diabetes enhances the production of matrix metallo-proteinases that lead to breakdown of collagen, potentially decreasing the mechanical stability of the plaque's fibrous cap. Overall, diabetes alters vascular smooth muscle function in ways that promote atherosclerotic lesion formation, plaque instability, and clinical events.21
It has been demonstrated that diabetic patients have a larger amount of lipid-rich plaques, which may be more prone to rupture.15 Moreover, recent observations have suggested that, in diabetic patients, human endothelial progenitor cells, which are supposed to be important regulators vascular repair, exhibit impaired proliferation, adhesion, and incorporation into vascular structures.22 In addition to the dysfunction described, the number of endothelial progenitor cells obtained from diabetic patients in culture was found to be reduced compared with age-and sex-matched control subjects, and the reduction was inversely related to HbA1c levels.23 An investigation documented that the level of endothelial progenitor cells was particularly low among diabetic patients with peripheral arterial disease (PAD) and hypothesized that depletion of this cell line may be involved in the pathogenesis of diabetic complications of the peripheral vasculature.24
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