Diabetes Mellitus and Ischemic Heart Disease: The Role of Ion Channels.

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Term Occurence Count Dictionary
type 2 diabetes mellitus 1 endocrinologydiseases
17β-estradiol 1 endocrinologydiseasesdrugs
Insulin 1 endocrinologydiseasesdrugs
diabetes mellitus 23 endocrinologydiseases
hyperglycemia 6 endocrinologydiseases
hyperinsulinemia 1 endocrinologydiseases
testosterone 1 endocrinologydiseasesdrugs

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Select Drug Character Offset Drug Term Instance
17β-estradiol 5119 Moreover, there are several hormones which contribute to coronary blood flow regulation. Among them, 17β-estradiol , progesterone, testosterone, antidiuretic hormone, and histamine determine vasodilatation [[7],[8],[9]],
Insulin 5308 vasodilatation [[7],[8],[9]], while growth hormone and angiotensin II are vasoconstrictors [[10]]. Insulin seems to have a double effect. It determines vasoconstriction, activating the sympathetic system, and
testosterone 5149 hormones which contribute to coronary blood flow regulation. Among them, 17β-estradiol, progesterone, testosterone , antidiuretic hormone, and histamine determine vasodilatation [[7],[8],[9]], while growth hormone and
Select Disease Character Offset Disease Term Instance
diabetes mellitus 14503 mediated by oxidative stress and inflammation, are the main substrates of coronary atherosclerosis in diabetes mellitus [[42]]. A complex network of signaling pathways is involved in the multistage pathological condition
diabetes mellitus 14863 atherosclerotic plaque [[43],[44]]. The nature of the hyperglycemic damage in patients affected by diabetes mellitus lies in the accumulation of superoxide anions, which are free radicals capable of activating cellular
diabetes mellitus 18562 apoptosis, and autonomic dysfunction are additional mechanisms responsible for cardiomyocyte changes in diabetes mellitus [[50],[52],[55],[56]]. In diabetes mellitus, chronic hyperglycemia plays a main role in the onset and
diabetes mellitus 18606 additional mechanisms responsible for cardiomyocyte changes in diabetes mellitus [[50],[52],[55],[56]]. In diabetes mellitus , chronic hyperglycemia plays a main role in the onset and progression of autonomic neuropathy, which
diabetes mellitus 19032 coronary atherosclerotic plaque represents a pathological process that is not uniquely associated with diabetes mellitus . In fact, other cardiovascular risk factors are involved in its pathogenesis. Although they all lead
diabetes mellitus 19220 pathogenesis. Although they all lead to the same final condition, they act in a different way compared to diabetes mellitus , for the purposes of atherosclerosis pathogenesis. Diabetes mellitus and all the consequences of the
diabetes mellitus 24010 international literature, the impairment of several ion channels has been associated with predisposition to diabetes mellitus . A study by Su et al. showed that AGEs could be able to cause vascular damage both in a direct and an
diabetes mellitus 27707 cause a dysregulation of channel activity, determining a higher or lower risk of developing type 2 diabetes mellitus —and, therefore, cardiovascular disease—in humans. The polymorphism Glu23Lys of KCNJ11 together with
diabetes mellitus 28144 suppression induced by glucose [[86]]. KCNJ11 and ABCC8 gain-of-function mutations relate to a rare type of diabetes mellitus , which arises before the first year of life: neonatal diabetes mellitus [[82]]. In this syndrome, the
diabetes mellitus 28216 mutations relate to a rare type of diabetes mellitus, which arises before the first year of life: neonatal diabetes mellitus [[82]]. In this syndrome, the increased K-ATP channel function determines reduced β cell depolarization,
diabetes mellitus 28718 in youth [[83]], a condition defined by the presence of lower blood glucose fasting levels than the diabetes mellitus threshold, but higher than normal ones [[90],[91]]. Furthermore, the rs5219 polymorphism only predisposes
diabetes mellitus 29265 Souza et al. demonstrated that the same polymorphism E23K (rs5219) was not associated with type 1 or 2 diabetes mellitus in Euro-Brazilian subjects [[94]]. A meta-analysis performed by Qin, L.J. et al. of KCNJ11 and ABCC8
diabetes mellitus 35257 the presence of IHD was observed [[11]]. On the other hand, no difference in terms of the presence of diabetes mellitus was observed between patients with CAD, microvascular dysfunction, and normal coronary arteries, giving
diabetes mellitus 36355 0.0001) and A/A (p = 0.0001), whereas rs5219 did not show any statistically significant correlation with diabetes mellitus . Moreover, in nondiabetic patients, rs5215_GG was more frequently associated with the presence of normal
diabetes mellitus 38244 provoke IHD independently from the presence of an atherosclerotic stenosis. In the determinism of IHD, diabetes mellitus is one of the strongest risk factors. However, the pathophysiology of myocardial ischemia in diabetic
diabetes mellitus 38900 pathophysiological role of SNPs of coronary artery and pancreas islet cell ion channels in the determinism of both diabetes mellitus and IHD. Through the systematic review of the most recent international literature, we highlighted that
diabetes mellitus 39102 we highlighted that there are some ion channels whose impaired function is strongly associated with diabetes mellitus and IHD susceptibility (Table 2). We also highlighted the most important SNPs that modify these channels’
diabetes mellitus 39620 CAD in Caucasians. Performing a post hoc analysis on subgroups of diabetic and nondiabetic patients, diabetes mellitus was not significantly associated with either acute coronary syndromes (i.e., ST elevation myocardial
diabetes mellitus 40040 observed clinical associations are in contrast with those classically described as associated with diabetes mellitus , which is one of the strongest risk factors for ACS, CAD, and microvascular dysfunction.Regarding genetic
diabetes mellitus 40373 absence of DM. Moreover, in our population, SNP rs5219 did not present any significant correlation with diabetes mellitus , different to observations made by some authors [[83],[92],[93],[95]]. Interestingly, in nondiabetic
diabetes mellitus 43670 they are closing. Cl−: Chloride.Figure 3Pathophysiology of atherogenesis in patients affected by diabetes mellitus . In diabetes, the combination of hyperglycemia, free fatty acid excess, and insulin resistance leads
diabetes mellitus 47075 youth-Different Authors do not agree about the presence or the absence of any significant correlation with diabetes mellitus -Predisposition to T2DM through reduced glucagon secretion suppression induced by glucose-Linkage disequilibrium
diabetes mellitus 48036 potassium channels. Nav: Voltage-gated sodium channel. SNPs: single-nucleotide polymorphisms. T2DM: Type 2 diabetes mellitus . BMI: body mass index. CAD: coronary artery disease
hyperglycemia 14231 by a state of long-standing insulin resistance with a compensatory hyperinsulinemia. Initially, the hyperglycemia remains under the threshold for the diagnosis of DM and it describes impaired glucose tolerance. Glucose
hyperglycemia 15273 oxidative stress through greater glucose oxidation in the citric acid cycle [[45]]. All these different hyperglycemia consequences lead to decreased cellular resistance to oxidative stress, amplification of the proinflammatory
hyperglycemia 17273 proposed pathophysiologic processes of diabetes-induced coronary microvascular dysfunction [[50]]. Both hyperglycemia and insulin resistance, besides tumor necrosis factor-α overexpression and inflammation, interfere
hyperglycemia 17836 arteries in diabetic subjects compared with a control group. These results suggest the role that chronic hyperglycemia might play in the pathogenesis of coronary microvascular dysfunction in diabetes [[53]]. Furthermore,
hyperglycemia 18633 for cardiomyocyte changes in diabetes mellitus [[50],[52],[55],[56]]. In diabetes mellitus, chronic hyperglycemia plays a main role in the onset and progression of autonomic neuropathy, which may reduce the vasodilator
hyperglycemia 43721 3Pathophysiology of atherogenesis in patients affected by diabetes mellitus. In diabetes, the combination of hyperglycemia , free fatty acid excess, and insulin resistance leads to several systemic effects, including increasing
hyperinsulinemia 14198 pathophysiological continuum, characterized by a state of long-standing insulin resistance with a compensatory hyperinsulinemia . Initially, the hyperglycemia remains under the threshold for the diagnosis of DM and it describes impaired
type 2 diabetes mellitus 27700 genes may cause a dysregulation of channel activity, determining a higher or lower risk of developing type 2 diabetes mellitus —and, therefore, cardiovascular disease—in humans. The polymorphism Glu23Lys of KCNJ11 together with

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