The role of advanced glycation end-products in the development of coronary artery disease in patients with and without diabetes mellitus: a review

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Term Occurence Count Dictionary
atorvastatin 2 endocrinologydiseasesdrugs
diabetes mellitus 3 endocrinologydiseases
glucose intolerance 1 endocrinologydiseases
hyperglycemia 9 endocrinologydiseases
hyperlipidemia 2 endocrinologydiseases
hyperuricemia 1 endocrinologydiseases
Sevelamer 1 endocrinologydiseasesdrugs
amyloidosis 1 endocrinologydiseases
pioglitazone 1 endocrinologydiseasesdrugs
osteoporosis 1 endocrinologydiseases
diabetic retinopathy 1 endocrinologydiseases
metformin 1 endocrinologydiseasesdrugs

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Sevelamer 37285 despite endogenous AGE production being the major source of circulating AGEs (Vlassara et al., [147]). Sevelamer carbonate, a compound frequently used in patients with advanced kidney disease as a phosphate binder,
atorvastatin 36165 the AGE/RAGE axis. Tam et al. reported an increase in esRAGE levels in patients with DM treated with atorvastatin , with a correlating decrease in LDL levels (Tam et al., [138]). In a rat model, atorvastatin treatment
atorvastatin 36258 treated with atorvastatin, with a correlating decrease in LDL levels (Tam et al., [138]). In a rat model, atorvastatin treatment for 24 weeks increased the serum and renal sRAGE levels and decreased renal RAGE expression
metformin 36607 been shown to reduce esRAGE levels with 6 months of treatment (Tan et al., [139]). In addition, both metformin and pioglitazone can block AGE formation in vitro (Rahbar et al.,[109]). ACE inhibitors and angiotensin
pioglitazone 36621 reduce esRAGE levels with 6 months of treatment (Tan et al., [139]). In addition, both metformin and pioglitazone can block AGE formation in vitro (Rahbar et al.,[109]). ACE inhibitors and angiotensin receptor blockers
Select Disease Character Offset Disease Term Instance
amyloidosis 30755 aggregates, linking RAGE mediated signaling to a number of pathogenic processes including neurodegeneration, amyloidosis , and tumor growth. By contrast, AGE binding to cell surface AGER1 inhibits these processes by suppressing
diabetes mellitus 144 advanced glycation end-products in the development of coronary artery disease in patients with and without diabetes mellitus : a reviewSarah Louise FishmanHalis SonmezCraig BasmanVarinder SinghLeonid PoretskyPublication date (epub):
diabetes mellitus 482 risk factors are insufficient to explain all cases of coronary artery disease (CAD) in patients with diabetes mellitus (DM). Advanced glycation end-products (AGEs) and their receptors may play important roles in the development
diabetes mellitus 2291 developing coronary artery disease (CAD) (Goff Jr et al., [48]; McClelland et al., [85]). Concurrent diabetes mellitus (DM) is known to confer additional risk. Multiple studies have demonstrated that glucose intolerance,
diabetic retinopathy 4241 “metabolic memory” has been supported by animal studies demonstrating continued progression of diabetic retinopathy despite correction of hyperglycemia (Engerman & Kern, [36]). In rats with induced diabetes, animals
glucose intolerance 2390 diabetes mellitus (DM) is known to confer additional risk. Multiple studies have demonstrated that glucose intolerance , insulin resistance, and hyperglycemia are associated with coronary artery disease pathogenesis (Turner
hyperglycemia 813 both micro-and macrovascular complications of diabetes has been observed with increased duration of hyperglycemia . This association persists even after glycemic control has been achieved, suggesting an innate mechanism
hyperglycemia 1086 that may serve as mediators of metabolic memory due to their increased production in the setting of hyperglycemia and generally slow turnover. Elevated AGE levels can lead to abnormal cross linking of extracellular
hyperglycemia 2435 additional risk. Multiple studies have demonstrated that glucose intolerance, insulin resistance, and hyperglycemia are associated with coronary artery disease pathogenesis (Turner et al., [141]; de Vegt et al., [29];
hyperglycemia 4284 by animal studies demonstrating continued progression of diabetic retinopathy despite correction of hyperglycemia (Engerman & Kern, [36]). In rats with induced diabetes, animals with poor glycemic control after 6 months
hyperglycemia 4945 of proteins, lipids, and nucleic acids. The formation of AGEs is enhanced in the presence of chronic hyperglycemia due to increased glucose availability. It has been hypothesized that early hyperglycemia leads to a
hyperglycemia 5034 of chronic hyperglycemia due to increased glucose availability. It has been hypothesized that early hyperglycemia leads to a proportional increase in AGE formation and oxidative stress. Over time, mitochondrial respiratory
hyperglycemia 5329 occurs leading to a self-perpetuating cycle of AGE formation and oxidative stress independently of hyperglycemia (Testa et al., [140]).AGEs have been linked to the aging process, the promotion of tumor metastasis,
hyperglycemia 7229 rate of AGE accumulation increases with advancing age, but is markedly increased in the presence of hyperglycemia , oxidative stress, and inflammation. AGE production and accumulation are stimulated by a variety of
hyperglycemia 10080 glucose metabolism in muscle and adipocytes, leading to reduced insulin mediated glucose uptake and hyperglycemia (Unoki et al., [142]). Increased AGE levels have been associated with many microvascular diabetic complications
hyperlipidemia 2115 who may benefit from invasive intervention.BackgroundIt has long been appreciated that age, gender, hyperlipidemia , hypertension, and smoking status contribute to the risk of developing coronary artery disease (CAD)
hyperlipidemia 13987 [72]). This association was independent of other risk factors for CAD including smoking, hypertension, hyperlipidemia , and hyperuricemia. In a large study of 1320 patients with type 2 DM, Lu et al. demonstrated that elevated
hyperuricemia 14007 was independent of other risk factors for CAD including smoking, hypertension, hyperlipidemia, and hyperuricemia . In a large study of 1320 patients with type 2 DM, Lu et al. demonstrated that elevated glycated albumin
osteoporosis 10813 of DM associated co-morbidities including non-alcoholic steatohepatitis (Hyogo & Yamagishi, [64]), osteoporosis (Wang et al., [151]) and polycystic ovarian syndrome (Merhi, [87]). Higher values of circulating CML

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