Diabetes abolishes the cardioprotection induced by sevoflurane postconditioning in the rat heart in vivo: Roles of glycogen synthase kinase-3β and its upstream pathways

Tai, Wenjun; Shi, Enyi; Yan, Long; Jiang, Xiaojing; Ma, Hong; Ai, Chunyu

doi:10.1016/j.jss.2012.02.021

Cited by 29 publications

(27 citation statements)

References 40 publications

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“…Raphael et al (2010) found that hyperglycemia abrogated the cardioprotection elicited by the inhaled anesthetic isoflurane, administered at the onset of myocardial reperfusion, using a rabbit in vivo model of acute ischemia/reperfusion injury, a finding that was associated with impaired activation of Akt-eNOS. Similarly, the infarct size-limiting effect of the inhaled anesthetics desflurane (Tai et al, 2012) and sevoflurane (Drenger et al, 2011), administered at the onset of myocardial reperfusion to rats in vivo, was abolished in the presence of diabetes. This was associated with a failure of these anesthetic agents to activate Akt, ERK1/2, GSK-3b (Tai et al, 2012), and STAT3 (Drenger et al, 2011).…”

Section: Diabetesmentioning

confidence: 99%

“…Similarly, the infarct size-limiting effect of the inhaled anesthetics desflurane (Tai et al, 2012) and sevoflurane (Drenger et al, 2011), administered at the onset of myocardial reperfusion to rats in vivo, was abolished in the presence of diabetes. This was associated with a failure of these anesthetic agents to activate Akt, ERK1/2, GSK-3b (Tai et al, 2012), and STAT3 (Drenger et al, 2011). An interesting study by Potier et al (2013) suggested that there may be differential effects in the response to cardioprotection using different bradykinin receptor agonists in the presence of diabetes.…”

Section: Diabetesmentioning

confidence: 99%

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Interaction of Risk Factors, Comorbidities, and Comedications with Ischemia/Reperfusion Injury and Cardioprotection by Preconditioning, Postconditioning, and Remote Conditioning

Ferdinándy¹,

Hausenloy²,

Heusch³

et al. 2014

Pharmacol Rev

508

499

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Section: Diabetesmentioning

confidence: 99%

Section: Diabetesmentioning

confidence: 99%

Interaction of Risk Factors, Comorbidities, and Comedications with Ischemia/Reperfusion Injury and Cardioprotection by Preconditioning, Postconditioning, and Remote Conditioning

Ferdinándy¹,

Hausenloy²,

Heusch³

et al. 2014

Pharmacol Rev

508

499

View full text Add to dashboard Cite

“…Moreover, it was also revealed in this study that the decrease in transient receptor potential cation channel subfamily V member 1 (TRPV1) and the increase in the expression of calcitonin gene related peptide (CGRP) and Substance P (SP) in diabetic hearts caused the loss of the cardioprotective activity of ischemic postconditioning associated with a failure to increase calcitonin gene related peptide (CGRP) and Substance P (SP) release [88]. Sevoflurane postconditioning was abolished by chemically induced diabetes in a rat model and this detrimental effect involved the impairment of phosphorylation of glycogen synthase kinase 3-beta (GSK-3 β ) and its upstream pathways, such as PI3 kinase/Akt and extracellular signal regulated kinases (ERK) in diabetes [89]. Najafi et al indicated that ischemic postconditioning did not exert a protective effect in diabetic hearts [90].…”

Section: Diabetes and Cardioprotective Strategiesmentioning

confidence: 99%

Experimental Diabetes Mellitus in Different Animal Models

Al-awar

Kupai

Veszelka

et al. 2016

Journal of Diabetes Research

212

211

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Animal models have historically played a critical role in the exploration and characterization of disease pathophysiology and target identification and in the evaluation of novel therapeutic agents and treatments in vivo. Diabetes mellitus disease, commonly known as diabetes, is a group of metabolic disorders characterized by high blood glucose levels for a prolonged time. To avoid late complications of diabetes and related costs, primary prevention and early treatment are therefore necessary. Due to its chronic symptoms, new treatment strategies need to be developed, because of the limited effectiveness of the current therapies. We overviewed the pathophysiological features of diabetes in relation to its complications in type 1 and type 2 mice along with rat models, including Zucker Diabetic Fatty (ZDF) rats, BB rats, LEW 1AR1/-iddm rats, Goto-Kakizaki rats, chemically induced diabetic models, and Nonobese Diabetic mouse, and Akita mice model. The advantages and disadvantages that these models comprise were also addressed in this review. This paper briefly reviews the wide pathophysiological and molecular mechanisms associated with type 1 and type 2 diabetes, particularly focusing on the challenges associated with the evaluation and predictive validation of these models as ideal animal models for preclinical assessments and discovering new drugs and therapeutic agents for translational application in humans.

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“…Activating ERK1/2 has been reported to participate in the cardioprotection of ischemic/pharmacological preconditioning/postconditioning against I/R injury [43,55,56,57]. However, diabetes inhibited the cardioprotection induced by preconditioning/postconditioning against I/R, which might be related to the reduced recovery of ERK1/2 [43,44,55]. In addition, Lambert et al studied how Na 2 S therapy attenuates I/R injury in an ERK1/2-dependent manner.…”

Section: Erk1/2 a Two-edged Sword In Dcm Developmentmentioning

confidence: 99%

The Role of ERK1/2 in the Development of Diabetic Cardiomyopathy

Sun

Tong

et al. 2016

IJMS

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Diabetes mellitus is a chronic metabolic condition that affects carbohydrate, lipid and protein metabolism and may impair numerous organs and functions of the organism. Cardiac dysfunction afflicts many patients who experience the oxidative stress of the heart. Diabetic cardiomyopathy (DCM) is one of the major complications that accounts for more than half of diabetes-related morbidity and mortality cases. Chronic hyperglycemia and hyperlipidemia from diabetes mellitus cause cardiac oxidative stress, endothelial dysfunction, impaired cellular calcium handling, mitochondrial dysfunction, metabolic disturbances, and remodeling of the extracellular matrix, which ultimately lead to DCM. Although many studies have explored the mechanisms leading to DCM, the pathophysiology of DCM has not yet been fully clarified. In fact, as a potential mechanism, the associations between DCM development and mitogen-activated protein kinase (MAPK) activation have been the subjects of tremendous interest. Nonetheless, much remains to be investigated, such as tissue- and cell-specific processes of selection of MAPK activation between pro-apoptotic vs. pro-survival fate, as well as their relation with the pathogenesis of diabetes and associated complications. In general, it turns out that MAPK signaling pathways, such as extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun N-terminal protein kinase (JNK) and p38 MAP kinase, are demonstrated to be actively involved in myocardial dysfunction, hypertrophy, fibrosis and heart failure. As one of MAPK family members, the activation of ERK1/2 has also been known to be involved in cardiac hypertrophy and dysfunction. However, many recent studies have demonstrated that ERK1/2 signaling activation also plays a crucial role in FGF21 signaling and exerts a protective environment of glucose and lipid metabolism, therefore preventing abnormal healing and cardiac dysfunction. The duration, extent, and subcellular compartment of ERK1/2 activation are vital to differential biological effects of ERK1/2. Moreover, many intracellular events, including mitochondrial signaling and protein kinases, manipulate signaling upstream and downstream of MAPK, to influence myocardial survival or death. In this review, we will summarize the roles of ERK1/2 pathways in DCM development by the evidence from current studies and will present novel opinions on “differential influence of ERK1/2 action in cardiac dysfunction, and protection against myocardial ischemia-reperfusion injury”.

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Diabetes abolishes the cardioprotection induced by sevoflurane postconditioning in the rat heart in vivo: Roles of glycogen synthase kinase-3β and its upstream pathways

Cited by 29 publications

References 40 publications

Interaction of Risk Factors, Comorbidities, and Comedications with Ischemia/Reperfusion Injury and Cardioprotection by Preconditioning, Postconditioning, and Remote Conditioning

Interaction of Risk Factors, Comorbidities, and Comedications with Ischemia/Reperfusion Injury and Cardioprotection by Preconditioning, Postconditioning, and Remote Conditioning

Experimental Diabetes Mellitus in Different Animal Models

The Role of ERK1/2 in the Development of Diabetic Cardiomyopathy

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