Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
There is accumulating evidence that the AGEs-RAGE interaction plays an important role in accelerated atherosclerosis in diabetes.
|
31378770 |
2019 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
However, the role of PKCδ in cardiac and mitochondrial dysfunction caused by AGE in diabetes is still unclear.
|
30090653 |
2018 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
AGE cannot replace HbA1c for the diagnosis and management of diabetes because there is no correlation of AGE with serum glucose, and because the half-life of protein with which glucose combines is only 14-20 days as compared to erythrocytes which have a half-life of 90-120 days.
|
30179123 |
2018 |
Diabetes
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Through the detection of protein expression, EGCG was observed to possess the ability to downregulate the accumulation of AGE-RAGE in pancreatic tissues as well as in the transcription factor nuclear factor-κB (NF-κB), which represents a potentially significant method by which EGCG influences diabetes.
|
30582209 |
2018 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
The objective of this study was to assess the validity of our experimental procedures for measuring AGEs in stored blood sample and to conduct a pilot study for developing AGE biomarkers for diabetes and/or age-related changes of glucose metabolism.
|
29718545 |
2018 |
Diabetes
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
In conclusion, these results suggest that AGE-induced activation of human umbilical vein endothelial cells promotes formation of endocan which is an endothelial dysfunction marker and may be related to vascular disease in diabetes.
|
25963575 |
2015 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Oral advanced glycation endproducts (AGEs) promote insulin resistance and diabetes by depleting the antioxidant defenses AGE receptor-1 and sirtuin 1.
|
22908267 |
2012 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
The receptor for AGE (RAGE) and AGE-receptor-1 (AGE-R1) are of particular interest, given that studies have demonstrated the deleterious effects of RAGE modulation and the protection afforded by AGE-R1 in the context of diabetes.
|
22250649 |
2012 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Stopping the vicious cycle of AGE-RAGE and RAGE axis signaling in the vulnerable heart and great vessels may be essential in controlling and preventing the consequences of diabetes.
|
20299674 |
2010 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
These results may partly explain the contribution of AGE-LDL and hSMC to the accelerated atherosclerosis in diabetes.
|
19818091 |
2010 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
A role for the soluble form of RAGE (sRAGE), which acts as a decoy for AGE, has been documented in patients with diabetes but no information is available in non-diabetic subjects.
|
18595673 |
2009 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Previous reports have suggested that levels of advanced glycation end product-modified LDL (AGE-LDL) increase in patients with diabetes due to elevated plasma glucose.
|
18164016 |
2008 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Although the time course, rate and extent of AGE generation and accumulation in diabetes and aging may be distinct, unifying outcomes of the ligand-RAGE interaction in the vasculature and heart are linked to upregulation of inflammatory and tissue-destructive mechanisms.
|
18331228 |
2007 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
Since a crosstalk between AGE and angiotensin II (Ang II) has been proposed in the pathogenesis of accelerated atherosclerosis in diabetes, we examined here whether and how telmisartan, a unique Ang II type 1 receptor blocker (ARB) with peroxisome proliferator-activated receptor-gamma (PPAR-gamma)-modulating activity, could inhibit AGE-induced CRP expression in a human hepatoma cell line, Hep3B cells.
|
17004092 |
2006 |
Diabetes
|
0.100 |
Biomarker
|
disease |
BEFREE |
The data suggest a significant suppression of angiogenesis by the retinal microvasculature during diabetes and implicate AGEs and AGE-receptor interactions in its causation.
|
15734857 |
2005 |