PPARγ–PI3K/AKT–NO signal pathway is involved in cardiomyocyte hypertrophy induced by high glucose and insulin

Peng, Xing; Chen, Rongchun; Wu, Yang; Huang, Bo; Tang, Cen; Chen, Jiafei; Wang, Qianqian; Wu, Qin; Yang, Junqing; Qiu, Hongmei; Jiang, Qingsong

doi:10.1016/j.jdiacomp.2015.04.012

Cited by 28 publications

(17 citation statements)

References 28 publications

(31 reference statements)

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“…However, iNOS is absent in healthy rat heart, while highly expressed under pathological conditions, such as ischemia, hyperglycemia, and inflammation . Increasing evidences suggested that phosphorylation of eNOS, the target of Akt, was an important downstream effector in survival signaling in cardiomyocytes . Raleigh et al demonstrated that recombinant human relaxin‐2 (serelaxin) protects myocardium against I‐R injury by eNOS activation, while eNOS knock out abolished serelaxin's beneficial effects.…”

Section: Discussionmentioning

confidence: 99%

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Hydromorphine postconditioning protects isolated rat heart against ischemia‐reperfusion injury via activating P13K/Akt/eNOS signaling

Liu

et al. 2018

Cardiovascular Therapeutics

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Summary Introduction Myocardial ischemia/reperfusion injury (myocardial I/R injury) has a high disability rate and mortality. Novel treatments for myocardial I/R injury are necessary. Aim In order to explore the protective effect of hydromorphine on myocardial I/R injury, we illuminate the underlying mechanism of the protective effect. Results Hydromorphine significantly reduced myocardial infarct size (IFN/AAR), CKMB (Creatine Kinase MB) and TN‐T (Troponin T) release, and improved cardiac function compared with I/R group. However, these advantageous effects were partly suppressed in the presence of hydromorphine. Myocardial I/R injury significantly decreased the phosphorylation of Akt and eNOS, and down‐regulated total nitric oxide and nitrotyrosine content, while these inhibitory effects were partly abolished by hydromorphine. Conversely, the activated effects of hydromorphine on the phosphorylation of Akt and eNOS, and NO release were totally reversed by LY294002, which, used individually, show the same influence on reperfusion injury. Conclusions These findings suggest that hydromorphine postconditioning may protect isolated rat heart against reperfusion injury via activating P13K/Akt/eNOS signaling.

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Section: Discussionmentioning

confidence: 99%

“…28 Increasing evidences suggested that phosphorylation of eNOS, the target of Akt, was an important downstream effector in survival signaling in cardiomyocytes. [29][30][31] Raleigh et al 32 to myocardial injury by nitrative stress. 35,36 Thereby, these findings may on account of different disease models, type, and dose of drugs.…”

Section: Discussionmentioning

confidence: 99%

Hydromorphine postconditioning protects isolated rat heart against ischemia‐reperfusion injury via activating P13K/Akt/eNOS signaling

Liu

et al. 2018

Cardiovascular Therapeutics

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“…Recent evidence shows that cardiac insulin signaling is hyperactive in a pathological hypertrophic model induced by pressure overload [55]. Genetic inhibition of the InsR-Akt1 signaling pathway substantially attenuates hypertrophy, adverse remodeling, and dysfunction following transverse aortic constriction [55, 59–62]. Thus, activation of InsR signaling in pressure overload model appears to promote detrimental pathological hypertrophy.…”

Section: Hyperinsulinemia Promotes Cardiac Remodeling: Hypertrophy Anmentioning

confidence: 99%

Insulin and β Adrenergic Receptor Signaling: Crosstalk in Heart

Wang

Xiang

2017

Trends in Endocrinology & Metabolism

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Recent advances show that insulin may affect β adrenergic receptor (βAR) signaling in heart, to modulate cardiac function in clinically relevant states such as diabetes and heart failure. Conversely, activation of βAR regulates cardiac glucose uptake and promotes insulin resistance in HF. We discussed recent characterization on the interaction between cardiac insulin receptor and βAR in myocardium, in which insulin stimulation cross talk with cardiac βAR via insulin receptor substrate-dependent and G protein receptor kinase 2-mediated phosphorylation of β2AR. The insulin-induced phosphorylation promotes β2AR coupling to Gi and expression of phosphodiesterase 4, which inhibit cardiac adrenergic signaling and compromise cardiac contractile function. These progresses might support new approaches for effectively prevention or treatment of obesity-or diabetes-related heart failure.

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“…Moreover, it was suggested that exosomal 15d-PGJ2 was already activated by PPAR-γ before entering recipient cells, because PPAR-γ was also enriched in exosomes from human plasma (Looze et al, 2009). Because PPARγ activation was demonstrated to attenuate cardiomyocyte hypertrophy induced by high glucose and insulin (Chen et al, 2015; Peng et al, 2015), exosomal 15d-PGJ2 is a promising strategy for preventing cardiomyopathy in patients with diabetes.…”

Section: Other Types Of Exosomal Cargoesmentioning

confidence: 99%

Exosomes: A Rising Star in Failing Hearts

Chen

Yang

2017

Front. Physiol.

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Although exosomes were previously recognized as a mechanism for discharging useless cellular components, growing evidence has elucidated their roles in conveying information between cells. They contribute to cell–cell communication by carrying nucleic acids, proteins and lipids that can, in turn, regulate behavior of the target cells. Recent research suggested that exosomes extensively participate in progression of diverse cardiovascular diseases (CVDs), such as myocardial infarction, cardiomyopathy, pulmonary arterial hypertension and others. Here, we summarize effects of exosome-derived molecules (mainly microRNAs and proteins) on cardiac function, to examine their potential applications as biomarkers or therapeutics in CVDs.

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PPARγ–PI3K/AKT–NO signal pathway is involved in cardiomyocyte hypertrophy induced by high glucose and insulin

Cited by 28 publications

References 28 publications

Hydromorphine postconditioning protects isolated rat heart against ischemia‐reperfusion injury via activating P13K/Akt/eNOS signaling

Hydromorphine postconditioning protects isolated rat heart against ischemia‐reperfusion injury via activating P13K/Akt/eNOS signaling

Insulin and β Adrenergic Receptor Signaling: Crosstalk in Heart

Exosomes: A Rising Star in Failing Hearts

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