Effects of liraglutide and ischemic postconditioning on myocardial salvage after I/R injury in pigs*

Ekström, Kathrine; Dalsgaard, Morten; Iversen, Kasper; Pedersen‐Bjergaard, Ulrik; Vejlstrup, Niels; Diemar, Sarah Seberg; Idorn, Manja; Thorsteinsson, Birger; Engstrøm, Thomas

doi:10.1080/14017431.2016.1197417

Cited by 10 publications

(10 citation statements)

References 20 publications

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“…In the past 20 years, with the maturity of technology, reperfusion therapy of PCI and thrombolysis treatment has been widely carried out all over the world and has become the main means of clinical treatment for AMI . Although timely and effective reperfusion therapy can save most of a damaged myocardium and improve cardiac function, reperfusion therapy will also accompany the occurrence of I/R damage . Reperfusion injury can cause cardiomyocyte death and irreversible impairment of cardiac function, and this process mainly occurs in the early stage of reperfusion therapy .…”

Section: Discussionmentioning

confidence: 99%

“…18 Although timely and effective reperfusion therapy can save most of a damaged myocardium and improve cardiac function, reperfusion therapy will also accompany the occurrence of I/R damage. 19 Reperfusion injury can cause cardiomyocyte death and irreversible impairment of cardiac function, and this process mainly occurs in the early stage of reperfusion therapy. 20 How to prevent and alleviate I/R injury of AMI has become an urgent problem to be solved.…”

Section: Discussionmentioning

confidence: 99%

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Inhibition of the LncRNA Gpr19 attenuates ischemia‐reperfusion injury after acute myocardial infarction by inhibiting apoptosis and oxidative stress via the miR‐324‐5p/Mtfr1 axis

et al. 2019

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Reperfusion therapy after acute myocardial infarction (AMI) can effectively restore the blood supply and nutritional support of ischemic myocardium and save the dying myocardium. However, myocardial ischaemia‐reperfusion (I/R) injury has become a new threat to reperfusion therapy for AMI. Many long‐chain noncoding RNAs (lncRNAs) are dysregulated by I/R damage. Of these dysregulated lncRNAs, Gpr19 was selected as a potential gene of interest based on its high expression change. We aimed to explore the functional role and molecular mechanism of Gpr19 in I/R injury of AMI. C57BL/6 mice underwent I/R injury as in vivo models. Neonatal rat ventricular cardiomyocytes (NRCMs) exposed to an oxygen glucose deprivation/recovery (OGD/R) system were used as an in vitro model. A TUNEL assay, western blot, and oxidative stress analysis were conducted in this study to determine apoptosis and oxidative stress levels. Our results indicated that inhibition of Gpr19 improves cardiac function and reduces apoptosis and myocardial fibrosis scar formation in vivo. Suppression of Gpr19 attenuates oxidative stress and apoptosis in NRCMs exposed to OGD/R. We further demonstrated that inhibition of Gpr19 decreases oxidative stress and apoptosis in OGD/R‐induced NRCMs by regulating miR‐324‐5p and mitochondrial fission regulator 1 (Mtfr1). We elucidated the functional role and potential molecular mechanism of Gpr19 in I/R injury of AMI, provided a theoretical basis for the importance of Gpr9 in I/R injury, and provided a new perspective for the clinical treatment of I/R injury of AMI.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Inhibition of the LncRNA Gpr19 attenuates ischemia‐reperfusion injury after acute myocardial infarction by inhibiting apoptosis and oxidative stress via the miR‐324‐5p/Mtfr1 axis

et al. 2019

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“…adenosine [452], glucagon-like peptide 1 analogs [121], metoprolol [217], and CsA [391]) in dogs and pigs. However, translation to clinical use has so far not been successful, and a consistent improvement of outcome in patients with STEMI has not yet been reported.…”

Section: Larger Mammal Hearts In Situmentioning

confidence: 99%

Practical guidelines for rigor and reproducibility in preclinical and clinical studies on cardioprotection

et al. 2018

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“…Data regarding the capacity of GLP-1 therapeutics to mitigate myocardial infarction remain equivocal because similar studies in swine from Kristensen et al (21) and Ekström et al (22) failed to show infarct mitigation, whereas Timmers et al (3) and others have demonstrated infarct reductions with GLP-1–based therapies. Similarly equivocal findings exist in rodent models as well, which show varied capacity for infarct mitigation (23,24).…”

Section: Discussionmentioning

confidence: 99%

Glucagon-Like Peptide 1 Receptor Activation Augments Cardiac Output and Improves Cardiac Efficiency in Obese Swine After Myocardial Infarction

et al. 2017

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This study tested the hypothesis that glucagon-like peptide 1 (GLP-1) therapies improve cardiac contractile function at rest and in response to adrenergic stimulation in obese swine after myocardial infarction. Obese Ossabaw swine were subjected to gradually developing regional coronary occlusion using an ameroid occluder placed around the left anterior descending coronary artery. Animals received subcutaneous injections of saline or liraglutide (0.005–0.015 mg/kg/day) for 30 days after ameroid placement. Cardiac performance was assessed at rest and in response to sympathomimetic challenge (dobutamine 0.3–10 μg/kg/min) using a left ventricular pressure/volume catheter. Liraglutide increased diastolic relaxation (dP/dt; Tau 1/2; Tau 1/e) during dobutamine stimulation (P < 0.01) despite having no influence on the magnitude of myocardial infarction. The slope of the end-systolic pressure volume relationship (i.e., contractility) increased with dobutamine after liraglutide (P < 0.001) but not saline administration (P = 0.63). Liraglutide enhanced the slope of the relationship between cardiac power and pressure volume area (i.e., cardiac efficiency) with dobutamine (P = 0.017). Hearts from animals treated with liraglutide demonstrated decreased β1-adrenoreceptor expression. These data support that GLP-1 agonism augments cardiac efficiency via attenuation of maladaptive sympathetic signaling in the setting of obesity and myocardial infarction.

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Effects of liraglutide and ischemic postconditioning on myocardial salvage after I/R injury in pigs*

Abstract: In our closed-chest pig-model, we were unable to detect any cardioprotective effect of liraglutide or ischemic postconditioning either alone or combined.

Cited by 10 publications

References 20 publications

Inhibition of the LncRNA Gpr19 attenuates ischemia‐reperfusion injury after acute myocardial infarction by inhibiting apoptosis and oxidative stress via the miR‐324‐5p/Mtfr1 axis

Inhibition of the LncRNA Gpr19 attenuates ischemia‐reperfusion injury after acute myocardial infarction by inhibiting apoptosis and oxidative stress via the miR‐324‐5p/Mtfr1 axis

Practical guidelines for rigor and reproducibility in preclinical and clinical studies on cardioprotection

Glucagon-Like Peptide 1 Receptor Activation Augments Cardiac Output and Improves Cardiac Efficiency in Obese Swine After Myocardial Infarction

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