Diabetes propels the risk for cardiovascular disease: sweet monocytes becoming aggressive?

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Term Occurence Count Dictionary
diabetes mellitus 1 endocrinologydiseases
hyperglycemia 25 endocrinologydiseases
hyperlipidemia 1 endocrinologydiseases
metformin 4 endocrinologydiseasesdrugs
obesity 1 endocrinologydiseases
type 2 diabetes mellitus 1 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
metformin 30613 has been shown to inhibit the process of trained immunity induced by β-glucan [[45]]. Interestingly, metformin treatment of T2D patients increases AMPK activation in monocyte-derived macrophages [[24]]. Moreover,
metformin 30725 treatment of T2D patients increases AMPK activation in monocyte-derived macrophages [[24]]. Moreover, metformin treatment reduced T2D monocyte activation, measured by a reduction in inflammasome activation and IL-1β
metformin 30890 a reduction in inflammasome activation and IL-1β secretion ex vivo [[24]]. These data suggest that metformin can reduce ‘training’ of monocytes that has initially been induced by a diabetic environment. Such
metformin 31071 by a diabetic environment. Such properties may contribute to the demonstrated beneficial effects of metformin on cardiovascular outcomes in patients with diabetes.In sum, the long-term reprogramming of monocytes
Select Disease Character Offset Disease Term Instance
diabetes mellitus 2167 leading cause of morbidity and mortality in individuals diagnosed with type 1 diabetes (T1D) or type 2 diabetes mellitus (T2D), as well as the entire population. Multiple risk factors have been described to contribute to
hyperglycemia 594 an important cardiovascular risk factor as shown by the observation that even transient periods of hyperglycemia , despite return to normoglycemia during follow-up, increase the risk for CVD, a phenomenon termed ‘hyperglycemic
hyperglycemia 982 atherosclerosis, we propose that long-term functional reprogramming of monocytes and macrophages, induced by hyperglycemia , plays an important role in the phenomenon of hyperglycemic memory leading to cardiovascular complications
hyperglycemia 1578 shift in cellular metabolism from oxidative phosphorylation to aerobic glycolysis. We hypothesize that hyperglycemia in diabetes patients induces long-term activation of monocytes and macrophages through similar mechanisms,
hyperglycemia 2467 and hypertension [[3]], which cause proatherogenic processes in diabetes patient’s independent of hyperglycemia . Nonetheless, several prospective studies have revealed that hyperglycemia per se, a defining characteristic
hyperglycemia 2542 patient’s independent of hyperglycemia. Nonetheless, several prospective studies have revealed that hyperglycemia per se, a defining characteristic of diabetes, is an important and independent risk factor for cardiovascular
hyperglycemia 2887 (HbA1c) levels is associated with a 31 % increase in cardiovascular events [[7]].The importance of hyperglycemia as a risk factor is also demonstrated by the observation that a period of elevated HbA1c levels in the
hyperglycemia 4324 ‘legacy effect’ [[8], [9]]. A growing body of evidence now suggests that adverse effects of prior hyperglycemia are ‘memorized’ by vascular cells or tissues over time, translating into an enhanced risk for CVD.
hyperglycemia 4847 reprogramming in gene expression without changing the nucleotide sequence of the DNA itself. Prior episodes of hyperglycemia associate with epigenetic changes in various vascular cell types in vitro and ex vivo (i.e., smooth
hyperglycemia 6094 and macrophages, defined as trained immunity. We finally propose that reprogramming of monocytes by hyperglycemia may contribute to the hyperglycemic memory as an inducer of vascular complications in patients with
hyperglycemia 7713 whether subsets of monocytes are affected in T1D patients, especially because animal studies show that hyperglycemia specifically increases inflammatory Ly6-Chi monocytes, whereas non-inflammatory Ly6-Clo monocytes were
hyperglycemia 8599 also affect monocyte number and function [[27]]. Therefore, to investigate the direct relation between hyperglycemia and monocyte activation, findings in T1D patient are easier to interpret. Monocytes from T1D patients
hyperglycemia 9184 others [[28]]. Importantly, the adhesion of monocytes to endothelial cells may depend on the level of hyperglycemia , since monocytes derived from poorly controlled diabetes patients show higher binding to endothelial
hyperglycemia 9927 independently of any other risk factors (e.g., plasma cholesterol levels), suggesting a direct link between hyperglycemia and plaque macrophage infiltration [[33]]. A recent study investigated expression of proinflammatory
hyperglycemia 10693 vitro cell culture studies have shed more light on possible mechanisms that may explain the effect of hyperglycemia on monocyte activation. Peritoneal macrophages isolated from T1D and T2D mouse models show increased
hyperglycemia 12151 stimuli, indicating a memorization of hyperglycemic events.Thus, there is strong evidence that chronic hyperglycemia , the hallmark of diabetes, is associated with a (low-grade) activation of the innate immune system,
hyperglycemia 12422 atherosclerosis. The phenomenon of hyperglycemic memory, i.e., the observation that even transient periods of hyperglycemia enhance development of atherosclerosis, suggests that elevated glucose may be somehow memorized and
hyperglycemia 20852 to training of cells by hyperglycemic conditions.Fig. 1Schematic representation of the concept that hyperglycemia induces ‘trained immunity’ in monocytes. Initial stimulation of monocytes by hyperglycemic conditions
hyperglycemia 23866 shown that long-term reprogramming of monocytes is mediated by epigenetic changes [[42], [43]]. Whether hyperglycemia induces similar “training” and epigenetic changes in innate immune cells driving atherosclerotic
hyperglycemia 24062 driving atherosclerotic development remains to be established. In mice, it has been shown that transient hyperglycemia induces H3K4me1 and reduces H3K9 demethylation in the promoter of the NF-κB in aortic endothelial cells,
hyperglycemia 24498 cell types, including vascular smooth muscle, retinal, and cardiac cells, respond to prior episodes of hyperglycemia with epigenetic changes [[12], [13], [62]]. Thus, strong evidence exists that hyperglycemic conditions
hyperglycemia 26789 were found, including changes in thioredoxin-interacting protein (TXNIP) known to be associated with hyperglycemia [[66]].While there is evidence that certain epigenetic changes occur in monocytes of patients with diabetes
hyperglycemia 28067 oxidative phosphorylation is mostly associated with an anti-inflammatory profile. Assuming that chronic hyperglycemia increases glucose availability as a substrate for innate immune cells, it could be hypothesized that
hyperglycemia 31319 shift in cellular metabolism from oxidative phosphorylation to aerobic glycolysis. We hypothesize that hyperglycemia in diabetes patients induces long-term activation of monocytes and macrophages through similar mechanisms,
hyperglycemia 32342 because of an imprinted proinflammatory response.While compelling new data suggest that this effect of hyperglycemia on long-term functional reprogramming of monocytes and macrophages is important in the pathophysiology
hyperglycemia 32663 life span of circulating monocytes ranges from days to weeks, while deleterious effects of exposure to hyperglycemia persist for years after implementation of improved glycemic control. It may well be that elevated glucose
hyperlipidemia 18703 diabetes. Shirai et al. revealed that various risk factors for coronary events, i.e., hypertension, hyperlipidemia , and T2D all correlated with IL-6 release by monocytes ex vivo, showing considerable potential for exploration
obesity 8440 endothelium [[26]]. T2D is frequently accompanied by multiple cardiovascular risk factors, such as obesity , dyslipidemia and/or high blood pressure, which also affect monocyte number and function [[27]]. Therefore,
type 2 diabetes mellitus 2160 the leading cause of morbidity and mortality in individuals diagnosed with type 1 diabetes (T1D) or type 2 diabetes mellitus (T2D), as well as the entire population. Multiple risk factors have been described to contribute to

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