Insights for Oxidative Stress and mTOR Signaling in Myocardial Ischemia/Reperfusion Injury under Diabetes.

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Term Occurence Count Dictionary
hyperinsulinemia 1 endocrinologydiseases
hyperlipidemia 1 endocrinologydiseases
metformin 8 endocrinologydiseasesdrugs
obesity 5 endocrinologydiseases
type 2 diabetes mellitus 1 endocrinologydiseases
diabetes mellitus 1 endocrinologydiseases
glucose intolerance 2 endocrinologydiseases
hyperglycemia 3 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
metformin 1299 diabetic heart, which interplays with oxidative stress directly or indirectly. Antihyperglycemic agent metformin and newly found free radicals scavengers, Sirt1 and CTRP9, may serve as promising pharmacological therapeutic
metformin 21795 cardioprotections against DM-induced MI/R injury are urgently needed.5.1. MetforminIt is well recognized that metformin could reduce cardiovascular end points of T2DM independently from its glucose-lowering effects. Administration
metformin 21919 cardiovascular end points of T2DM independently from its glucose-lowering effects. Administration of metformin significantly attenuates I/R injury via relieving ER stress [[105]] and activating of AMPK-eNOS prosurvival
metformin 22143 pathway in both nondiabetic and diabetic mice [[105], [106]]. However, further research demonstrated that metformin effectively attenuated LV hypertrophy and dysfunction by activating mTOR, p70S6K (Thr389), and S6 phosphorylation
metformin 22322 mTOR, p70S6K (Thr389), and S6 phosphorylation in both wild-type and AMPKα2 KO mice, suggesting that metformin attenuated myocardial mTOR signaling independently of AMPKα2 activation [[107]]. Metformin reduces
metformin 22817 factor (bFGF) in the circulation and the myocardium [[110], [111]]. As a routine oral agent for T2DM, metformin might be a potential pharmacological therapeutic target to protect against MI/R injury under diabetes
metformin 29036 demonstrated clinically effective against cardiac injury in diabetic population. Antihyperglycemic agent metformin and newly found free radicals scavengers, Sirt1 and CTRP9, may serve as promising pharmacological cardiometabolic
metformin 34666 et al. [[78]]AMPKα2 knockout miceMetformin (100 mg/kg/day, gavage) for 3 weeksAdministration of metformin was effective in attenuating TAC-induced LV remodeling in both wild-type and AMPKα2 knockout mice and
Select Disease Character Offset Disease Term Instance
diabetes mellitus 6556 suppression of ER stress could reduce myocardial infarction (MI) size in high fat diet- (HFD-) induced type 2 diabetes mellitus (T2DM) [[32]]. Our recent study found that preconditioning of C1q/TNF-related protein (CTRP) 9, a newly
glucose intolerance 24666 actions. Increasing the circulating CTRP9 level is a beneficial action against HFD-induced obesity and glucose intolerance [[118]], whereas CTRP9-deficiency mice performed exacerbated insulin resistance [[119]]. Importantly,
glucose intolerance 27025 found that administration of rapamycin for two weeks could enhance the insulin level, leading to a glucose intolerance and insulin resistance in mice. However, more than six weeks treatment could improve insulin sensitivity
hyperglycemia 8440 increased ROS and/or inadequate antioxidant defenses [[45]]. It develops directly or indirectly from hyperglycemia , hyperlipidemia, and insulin resistance under DM [[15], [46]] and in turn, disturbs metabolic hemostasis
hyperglycemia 10278 [[49]]. H2O2 is more likely converted to ∙OH other than scavenged by CAT or GPx [[50]]. Moreover, hyperglycemia increases cardiac free fatty acid (FFA) levels, which extensively leads to a great rise of ROS formation
hyperglycemia 14494 increase of mTORC1 activity in T2DM causes insulin resistance, which contributes to hyperinsulinemia and hyperglycemia [[79]–[81]]. Evidences showed that mTORC1 was activated in the hearts of obese and diabetic animals
hyperinsulinemia 14473 SignalingChronic increase of mTORC1 activity in T2DM causes insulin resistance, which contributes to hyperinsulinemia and hyperglycemia [[79]–[81]]. Evidences showed that mTORC1 was activated in the hearts of obese and
hyperlipidemia 8455 and/or inadequate antioxidant defenses [[45]]. It develops directly or indirectly from hyperglycemia, hyperlipidemia , and insulin resistance under DM [[15], [46]] and in turn, disturbs metabolic hemostasis and impairs
obesity 14690 and diabetic animals during reperfusion, increasing the vulnerability of MI/R injury. In HFD-induced obesity mice, cardiac autophagosome formation was decreased, accompanied by cardiac dysfunction, which could
obesity 17063 I/R-induced inflammation and necrosis, inhibited cardiac fibrosis in adverse LV remodeling in diet-induced obesity mice [[89]]. They demonstrated that Akt phosphorylation was higher in mTOR overexpressed mice than WT
obesity 24502 therapeutic target for MI/R injury under DM.5.3. CTRP9CTRP9 is a newly found APN paralog. It protects against obesity and T2DM through anti-inflammation and antiapoptotic actions. Increasing the circulating CTRP9 level
obesity 24654 antiapoptotic actions. Increasing the circulating CTRP9 level is a beneficial action against HFD-induced obesity and glucose intolerance [[118]], whereas CTRP9-deficiency mice performed exacerbated insulin resistance
obesity 31643 recovery and had less of the necrotic markers CK and LDH subjected to I/R injury in high fat diet-induced obesity CardioprotectivePark et al. [[69]]Diabetic mice induced by STZRapamycin (5 mg/kg i.v.) 10 min before
type 2 diabetes mellitus 6549 suppression of ER stress could reduce myocardial infarction (MI) size in high fat diet- (HFD-) induced type 2 diabetes mellitus (T2DM) [[32]]. Our recent study found that preconditioning of C1q/TNF-related protein (CTRP) 9, a newly

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