Role of Advanced Glycation End Products on Aortic Calcification in Patients with Type 2 Diabetes Mellitus

Abstract

The aim of this study was to evaluate the relationship between serum levels of advanced glycation end products (AGEs) and abdominal aortic calcification (AAC) in patients with type 2 diabetes mellitus (DM2). This was a prospective cross-sectional study. One-hundred and four consecutive patients with DM2 were given lateral lumbar X-rays in order to quantify abdominal aortic calcification (AAC). Circulating levels of AGEs and classical cardiovascular risk factors were determined. Clinical history was also registered. Patients with higher AGEs values had higher grades of aortic calcification and higher numbers of diabetic-related complications. Multivariate logistic regression analysis showed that being older, male and having high levels of AGEs and triglycerides were the independent risk factors associated to moderate-severe AAC when compared to no-mild AAC. Our results suggest that AGEs plays a role in the pathogenesis of aortic calcifications. In addition, the measurement of AGEs levels may be useful for assessing the severity of AAC in the setting of diabetic complications.

Smooth muscle NF90 deficiency ameliorates diabetic atherosclerotic calcification in male mice via FBXW7-AGER1-AGEs axis

“…2a ). Studies have demonstrated that the AGE-RAGE signaling pathway is closely associated with the pathogenesis of diabetic vascular calcification 1 , 6 . So, we chose AGE-RAGE signaling pathway-associated proteins for further study.…”

“…The mechanisms have been raised to state how AGEs accelerate atherosclerotic calcification in diabetes. On the one hand, chronically elevated hyperglycemia markedly accelerated the AGEs production 6 , on the other hand, hyperglycemia specifically impaired the clearance of AGEs 38 . Excessive accumulation of AGEs activates RAGE, and accelerates atherosclerotic calcification by modifying phenotype switch of VSMC from contractile to osteoblastic phenotype, apoptosis and MV release 11 , 26 .…”

“…Several factors underlying DM play a pivotal role in atherosclerotic calcification including inflammation, oxidative stress, advanced glycation end products (AGEs), and inorganic phosphate 1 – 5 . The prolonged accumulation of hyperglycemia-induced AGEs may be closely associated with the pathogenesis of aortic calcification in patients with DM 1 , 6 . However, the mechanisms underlying this association remain unclear.…”

“…AGEs are a group of heterogeneous compounds formed from proteins or lipids with glucose via Amadori reactions or non-enzymatic glycosylation reactions during DM or from foods prepared at high temperatures 1 , 6 . The accumulation of AGEs promotes oxidative stress, inflammation, and contributes to vascular complications in DM 7 .…”

The Role of Advanced Glycation End-Product Levels Measured by Skin Autofluorescence in the Development of Mitral Annular Calcification

“…This also leads to an increase in the production and accumulation of AGEs in the existing tissue, which contributes to the current situation. Sanchis et al and Deng et al also blamed this mechanism in their studies, which showcased the relationship between aortic valve calcification and serum AGE levels [ 28 , 29 ]. We also believe that the increase in AGE levels in our study affects the development of MAC by using similar mechanisms.…”