Invited commentary

Abstract

Understanding the pathophysiology of abdominal aortic aneurysms (AAA) is necessary in order to characterize predictive factors for AAA and develop pharmaceutical interventions to slow AAA progression. Diabetes is an important factor that has been noticed to be negatively associated with AAA development and progression. The growth rates and incidence of AAA rupture in patients with diabetes are significantly lower than in AAA patients without diabetes. Finding the mechanism of this negative association could bring us closer to prevention of AAA development. The development of atherosclerosis in the diabetic vasculature has been associated with advanced glycation end products (AGEs). AGEs can cause vascular complications by forming cross-links between molecules in the extracellular matrix (ECM), permanently altering cellular structure. ECM changes are proposed to play a role in the pathophysiology of AAA as well. It has been published that AGEs may stimulate AAA formation by promoting metalloproteinase-9 expression. However, the exact role of AGEs in AAA development and its association with diabetes is unknown. The study of Moll et al showed that the concentration of cross-linking AGE pentosidine was increased in AAA wall biopsy specimens in patients with diabetes compared with nondiabetic patients. The pentosidine concentration was lower in larger aneurysms of diabetic patients, whereas ex vivo glycated AAA biopsy specimens were resistant against proteolytic breakdown of collagen. Why cross-linking AGEs contribute to vascular complications in diabetes but are negatively associated with AAA remains a question. Do the changes by cross-linking AGEs in the ECM contribute to atherosclerosis in small vessels and reinforce the ECM in AAA in patients with diabetes? The difference between diabetic and nondiabetic patients with AAA requires more investigation to understand the underlying protective mechanism of diabetes from AAA progression. At the same time, the cardiovascular burden in diabetic patients is higher, which raises the question about whether we should postpone AAA repair in diabetic patients. A potential role for glycated cross-links in abdominal aortic aneurysm diseaseJournal of Vascular SurgeryVol. 65Issue 5PreviewDiabetes is a risk factor for atherosclerotic disease but negatively associated with the development and progression of abdominal aortic aneurysm (AAA). Advanced glycation end products (AGEs) are increased in diabetes and renders the vascular matrix more resistant to proteolysis. We assessed the concentration of AGEs in AAA biopsies obtained from diabetic and nondiabetic patients and hypothesized that (nonenzymatic) glycation of AAA tissue protects against proteolytic breakdown of collagen. Full-Text PDF Open Archive