Role of insulin receptors in myocardial ischaemia-reperfusion injury during cardiopulmonary bypass

Liang, Guiyou; Wu, Haoyue; Li, Jian; Cai, Qingyong; Gao, Zhengyu

doi:10.1080/ac.66.3.2114132

Cited by 9 publications

(16 citation statements)

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“…Severe cardiac injury and cardiac dysfunction are the main consequences of CPB surgery . Consistent with these findings, our data showed that the levels of cardiac injury biomarkers, including plasma creatine kinase MB and troponin I, significantly elevated 2 hours after CPB (Figure A,B).…”

Section: Resultssupporting

confidence: 87%

Activation of AMPK alleviates cardiopulmonary bypass‐induced cardiac injury via ameliorating acute cardiac glucose metabolic disorder

Wang

Cao

Yin

et al. 2018

Cardiovascular Therapeutics

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Summary Recent years, studies have demonstrated that hyperglycemia is one of the main manifestations after cardiac surgeries, which contributes to myocardial injuries and increases the chance of subsequent complications and mortality in such patients. However, strategies targeting at glucose metabolic disorder after cardiac surgeries to attenuate myocardial injuries are inadequately studied. In this study, a rat model of cardiopulmonary bypass (CPB) was applied to investigate the role of Adenosine 5'‐monophosphate‐activated protein kinase (AMPK) in modulating myocardial glucose metabolic‐induced cardiac injuries after cardiac surgery. The results revealed that CPB elicited significant cardiac dysfunction, and pronouncedly elevated the markers of myocardial injuries including serum creatine kinase MB and cardiac troponin I. Additionally, blunted myocardial glucose uptake after CPB was associated with decreased membrane glucose transporter 4 (GLUT4) content. However, pretreatment of AMPK agonist 5‐aminoimidazole‐4‐carboxamide1‐β‐D‐ribofuranoside (AICAR) at the beginning of CPB activated AMPK, enhanced phosphorylation of Akt substrate 160 (AS160), and increased myocardial membrane content of GLUT4. Meanwhile, improved myocardial glucose uptake and more importantly alleviated cardiac injury were also observed after CPB pretreated with AICAR. Moreover, the application of a mutant form of AS160 (AS160‐4P) abolished the beneficial effect of AICAR, as evidenced by impaired cardiac glucose uptake, reduced myocardial membrane GLUT‐4 translocation, increased cardiac injury markers, and deterioration of cardiac function after CPB. In conclusion, it was suggested in this study that preactivation of AMPK by AICAR improved myocardial glucose uptake by promoting AS160 dependent myocardial membrane GLUT‐4 translocation, which ultimately provided a potent cardioprotective effect.

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Section: Resultssupporting

confidence: 87%

Activation of AMPK alleviates cardiopulmonary bypass‐induced cardiac injury via ameliorating acute cardiac glucose metabolic disorder

Wang

Cao

Yin

et al. 2018

Cardiovascular Therapeutics

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“…The lungs are one of the most vulnerable solid organs. There are several clinical conditions wherein IR-induced ALI is implicated [ 45 – 47 ]. Numerous attempts have been made to preserve lung viability after lung transplantation, pulmonary thrombo-embolectomy, or cardio-pulmonary by-pass [ 45 – 47 ].…”

Section: Discussionmentioning

confidence: 99%

Anti-Vascular Endothelial Growth Factor Antibody Suppresses ERK and NF-κB Activation in Ischemia-Reperfusion Lung Injury

et al. 2016

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Ischemia-reperfusion (IR)-induced acute lung injury (ALI) is implicated in several clinical conditions like lung transplantation, acute pulmonary embolism after thrombolytic therapy, re-expansion of collapsed lung from pneumothorax or pleural effusion, cardiopulmonary bypass and etc. Because mortality remains high despite advanced medical care, prevention and treatment are important clinical issues for IR-induced ALI. Vascular endothelial growth factor (VEGF) has a controversial role in ALI. We therefore conducted this study to determine the effects of anti-VEGF antibody in IR-induced ALI. In the current study, the IR-induced ALI was conducted in a rat model of isolated-perfused lung in situ in the chest. The animals were divided into the control, control + preconditioning anti-VEGF antibody (bevacizumab, 5mg/kg), IR, IR + preconditioning anti-VEGF antibody (1mg/kg), IR+ preconditioning anti-VEGF antibody (5mg/kg) and IR+ post-IR anti-VEGF antibody (5mg/kg) group. There were eight adult male Sprague-Dawley rats in each group. The IR caused significant pulmonary micro-vascular hyper-permeability, pulmonary edema, neutrophilic infiltration in lung tissues, increased tumor necrosis factor-α, and total protein concentrations in bronchoalveolar lavage fluid. VEGF and extracellular signal-regulated kinase (ERK) were increased in IR-induced ALI. Administration of preconditioning anti-VEGF antibody significantly suppressed the VEGF and ERK expressions and attenuated the IR-induced lung injury. This study demonstrates the important role of VEGF in early IR-induced ALI. The beneficial effects of preconditioning anti-VEGF antibody in IR-induced ALI include the attenuation of lung injury, pro-inflammatory cytokines, and neutrophilic infiltration into the lung tissues.

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“…However, beta cells secretory granules was affected under condition of poor perfusion, oxidative stress, or infections, which might change the process of converting pro-insulin to insulin and C-peptide and further result in pancreatic beta cells dysfunction. 14 , 15 …”

Section: Discussionmentioning

confidence: 99%

Relationship Between Beta Cell Dysfunction and Severity of Disease Among Critically Ill Children

Lu²,

Xiao³

et al. 2016

Medicine

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Although beta cell dysfunction has been proved to predict prognosis among humans and animals, its prediction on severity of disease remains unclear among children. The present study was aimed to examine the relationship between beta cell dysfunction and severity of disease among critically ill children.This prospective study included 1146 critically ill children, who were admitted to Pediatric Intensive Care Unit (PICU) of Hunan Children's Hospital from November 2011 to August 2013. Information on characteristics, laboratory tests, and prognostic outcomes was collected. Homeostasis model assessment (HOMA)-β, evaluating beta cell function, was used to divide all participants into 4 groups: HOMA-β = 100% (group I, n = 339), 80% ≤ HOMA-β < 100% (group II, n = 71), 40% ≤ HOMA-β < 80% (group III, n = 293), and HOMA-β < 40% (group IV, n = 443). Severity of disease was assessed using the worst Sequential Organ Failure Assessment (SOFA) score, Pediatric Risk of Mortality (PRISM) III score, incidence of organ damage, septic shock, multiple organ dysfunction syndrome (MODS), mechanical ventilation (MV) and mortality. Logistic regression analysis was used to evaluate the risk of developing poor outcomes among patients in different HOMA-β groups, with group I as the reference group.Among 1146 children, incidence of HOMA-β < 100% was 70.41%. C-peptide and insulin declined with the decrement of HOMA-β (P < 0.01). C-reactive protein and procalcitonin levels, rather than white blood cell, were significantly different among 4 groups (P < 0.01). In addition, the worst SOFA score and the worst PRISMIII score increased with declined HOMA-β. For example, the worst SOFA score in group I, II, III, and IV was 1.55 ± 1.85, 1.71 ± 1.93, 1.92 ± 1.63, and 2.18 ± 1.77, respectively. Furthermore, patients with declined HOMA-β had higher risk of developing septic shock, MODS, MV, and mortality, even after adjusting age, gender, myocardial injury, and lung injury. For instance, compared with group I, the multivariate-adjusted odds ratio (95% confidence interval) for developing septic shock was 2.17 (0.59, 8.02), 2.94 (2.18, 6.46), and 2.76 (1.18, 6.46) among patients in group II, III, and IV, respectively.Beta cell dysfunction reflected the severity of disease among critically ill children. Therefore, assessment of beta cell function is critically important to reduce incidence of adverse events in PICU.

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Role of insulin receptors in myocardial ischaemia-reperfusion injury during cardiopulmonary bypass

Cited by 9 publications

References 0 publications

Activation of AMPK alleviates cardiopulmonary bypass‐induced cardiac injury via ameliorating acute cardiac glucose metabolic disorder

Activation of AMPK alleviates cardiopulmonary bypass‐induced cardiac injury via ameliorating acute cardiac glucose metabolic disorder

Anti-Vascular Endothelial Growth Factor Antibody Suppresses ERK and NF-κB Activation in Ischemia-Reperfusion Lung Injury

Relationship Between Beta Cell Dysfunction and Severity of Disease Among Critically Ill Children

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