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Some clinical studies demonstrated that high AGEs levels were associated with the risk of CVD [ 34, 35].
Therefore, we hypothesize that inflammatory responses in AOSD may be related to high AGEs levels and/or low sRAGE levels, which may lead to enhanced production of inflammatory mediators.
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High AGE levels in mothers predict lower adiponectin and higher plasma insulin levels or homeostasis model assessment (HOMA).
High AGE levels are associated with increased mortality rates in flies and thus are classified as biomarkers of aging and oxidative stress damage in Drosophila (Chakravarti & Chakravarti, 2007; Jacobson et al., 2010).
High AGE levels (over the median value) 5-fold increased the risk of post-infarction HF during the follow-up period, regardless of age, DM presence and glycaemic control, infarct's seriousness (ventricle dysfunction and troponin elevation) and other biomarkers such as NT-proBNP.
Significantly higher AGEs levels were also observed in active AOSD patients compared with inactive AOSD patients or inactive SLE patients.
As shown in Figure 1A and Table 2, significantly higher AGEs levels were observed in active AOSD patients and active SLE patients than the levels in healthy subjects.
In comparison to AOSD patients with monocyclic pattern, significantly higher AGEs levels were observed in those with polycyclic or chronic articular pattern.
The highest AGE levels are found in tissues with the slowest turnover such as skin, tendon, bone, amyloid plagues, and cartilage (19).
AGER1 correlated with serum AGE levels in normal individuals, but patients with diabetic or nondiabetic chronic kidney disease had lower monocyte AGER1 despite higher AGE levels, suggesting a potential therapeutic target.
Potential mechanisms through which AGEs could lead to the development of CAC are via low-grade inflammation (LGI) and endothelial dysfunction (ED), which are both associated with higher AGE levels [ 3].
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