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STZ-induced diabetes increases atherosclerotic plaque area by four- to fivefold in the aorta of apo-E deficient mice (72,84,85). Treatment of diabetic apo-E -/- mice with the ACE inhibitor perindopril reduces lesion area, macrophage infiltration, and collagen content (85). A similar reduction in aortic plaque area was observed in STZ-induced diabetic apo-E-deficient mice treated with the AT1 receptor antagonist Irbesartan (72). Both ACE and AT1 receptor expression are increased in aortic lesions in the diabetic apo-E-deficient mice, suggesting that the Ang II/AT1 pathway is upregulated within the atherosclerotic plaque and contributing to the accelerated lesion formation in this model. Multiple factors may contribute to the increased expression of ACE and the AT1 receptor in athersclerotic lesions in diabetes. As previously mentioned, hyperglycemia can increase both Ang II production and AT1 expression (64,65). Alternatively, the upregulation of AT1 receptor expression could be mediated by diabetes-induced inflammation. Elevated levels of C-reactive protein (CRP) have been associated with atherosclerosis in diabetic patients (86) and transgenic overexpression of CRP in apo-E-deficient mice induces a sixfold increase of AT1 receptor expression in atherosclerotic lesions (87). Moreover, ACE inhibition, AT1 receptor antagonism, and genetic tissue ACE deficiency decrease atherosclerotic lesion area in apo-E-deficient mice in the absence of diabetes (88,89), showing that the RAS promotes atherosclerosis in both the absence or presence of diabetes.

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