Crosstalk between GSK-3β-actuated molecular cascades and myocardial physiology

Sharma, Arun Kumar; Bhatia, Saurabh; Al‐Harrasi, Ahmed; Nandave, Mukesh; Hagar, Hanan

doi:10.1007/s10741-020-09961-9

Cited by 20 publications

(7 citation statements)

References 65 publications

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“…Notably, our results showed that CD47 expression decreased after GSK-3β inhibition. The roles of GSK-3β in cardiac biology are well recognized ( Beurel et al, 2015 ; Lal et al, 2015 ; Zhou et al, 2016 ; Sharma et al, 2020 ). GSK-3β is involved in the development of many cardiovascular diseases via multiple signal transduction pathways, such as Wnt/β-catenin ( Guo et al, 2012 ), TGF-β1-SMAD-3 ( Jope et al, 2007 ; Lal et al, 2014 ) and apoptosis ( Lal et al, 2015 ; Su et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Targeting Glycogen Synthase Kinase 3 Beta Regulates CD47 Expression After Myocardial Infarction in Rats via the NF-κB Signaling Pathway

Wang

et al. 2021

Front. Pharmacol.

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The aim of this study was to investigate the effects of the GSK-3β/NF-κB pathway on integrin-associated protein (CD47) expression after myocardial infarction (MI) in rats. An MI Sprague Dawley rat model was established by ligating the left anterior descending coronary artery. The rats were divided into three groups: Sham, MI, and SB + MI (SB216763) groups. Immunohistochemistry was used to observe the changes in cardiac morphology. A significant reduction in the sizes of fibrotic scars was observed in the SB + MI group compared to that in the MI group. SB216763 decreased the mRNA and protein expression of CD47 and NF-κB during MI. Primary rat cardiomyocytes (RCMs) and the H9c2 cell line were used to establish in vitro hypoxia models. Quantitative real-time PCR and western blotting analyses were conducted to detect mRNA and protein expression levels of CD47 and NF-κB and apoptosis-related proteins, respectively. Apoptosis of hypoxic cells was assessed using flow cytometry. SB216763 reduced the protein expression of CD47 and NF-κB in RCMs and H9c2 cells under hypoxic conditions for 12 h, and alleviated hypoxia-induced apoptosis. SN50 (an NF-κB inhibitor) also decreased CD47 protein expression in RCMs and H9c2 cells under hypoxic conditions for 12 h and protected cells from apoptosis. GSK-3β upregulates CD47 expression in cardiac tissues after MI by activating NF-κB, which in turn leads to myocardial cell damage and apoptosis.

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Section: Discussionmentioning

confidence: 99%

Targeting Glycogen Synthase Kinase 3 Beta Regulates CD47 Expression After Myocardial Infarction in Rats via the NF-κB Signaling Pathway

Wang

et al. 2021

Front. Pharmacol.

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“…The possibility of using GSK3b as a therapeutic target for cardiomyocyte protection has attracted considerable attention [129][130][131][132] . Earlier studies reported a causative role for GSK3b in the necrosis and apoptosis of cardiomyocytes [129] and a protective role against cardiac fibrosis [130] .…”

Section: Doxorubicin-induced Cardiotoxicitymentioning

confidence: 99%

“…This is associated with reduced phosphorylation of p53, heat shock factor-1, and myeloid cell leukemia sequence-1, and inhibition of Bax translocation [129] . Subsequent studies showed the effect of targeting GSK3b on the maintenance of myocardial homeostasis, as well as the therapeutic effects of GSK3b inhibition against diabetes-associated myocardial injury and experimentally induced myocardial infarction [131,132] . A recent study demonstrated that GSK3b inhibition ameliorates triptolide-induced acute cardiac injury in rodents by desensitizing the mitochondrial permeability transition [133] .…”

Section: Doxorubicin-induced Cardiotoxicitymentioning

confidence: 99%

Glycogen synthase kinase 3β biology in bone and soft tissue sarcomas

Abe¹,

Shimozaki²,

Domoto³

et al. 2020

JCMT

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“…But whether SIRT1 participating in EPI-inhibited cardiac brosis is unclear. Glycogen synthase kinase-3β (GSK-3β), a member of serine/threonine kinase family which regulated various cellular physiology [14]. Meantime, GSK-3β played an important role in cardiac physiology.…”

Section: Introductionmentioning

confidence: 99%

“…Moreover, GSK-3β could be phosphorylated by AKT (protein kinase B, a multifunctional protein kinase), which showed cardioprotective effect [14]. Therefore, our aim was to evaluate the protective effect of EPI on cardiac brosis and elucidate the exact mechanism.…”

Section: Introductionmentioning

confidence: 99%

(-)-Epicatechin Inhibits Cardiac Fibrosis via SIRT1/AKT/GSK3β Pathway

Guo

Luo

Wang

et al. 2021

Preprint

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Background: (-)-Epicatechin (EPI) is an important substance involved in protective effects of flavanol-rich foods. Many studies indicate EPI has cardioprotective effect, but the effect of EPI in inhibition of cardiac fibrosis is unclear. Thus, we aimed to evaluate the effect of EPI in preventing cardiac fibrosis and unveil the molecular mechanisms. Methods: Cardiac fibrosis model was established by transaortic constriction (TAC). The acutely isolated cardiac fibroblasts were induced to myofibroblasts with angiotensin II (AngII). Results: EPI markedly attenuated TAC-induced cardiac dysfunction and fibrosis in mice. In cultured CFs, EPI blocked AngII-induced myofibroblast transformation and collagen production. Furthermore, EPI conducted anti-fibrotic effects by activating the the SIRT1/AKT/GSK3β pathway. Conclusions: These findings will supply new agent and mechanism of action for treating cardiac fibrosis in the future.

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Crosstalk between GSK-3β-actuated molecular cascades and myocardial physiology

Cited by 20 publications

References 65 publications

Targeting Glycogen Synthase Kinase 3 Beta Regulates CD47 Expression After Myocardial Infarction in Rats via the NF-κB Signaling Pathway

Targeting Glycogen Synthase Kinase 3 Beta Regulates CD47 Expression After Myocardial Infarction in Rats via the NF-κB Signaling Pathway

Glycogen synthase kinase 3β biology in bone and soft tissue sarcomas

(-)-Epicatechin Inhibits Cardiac Fibrosis via SIRT1/AKT/GSK3β Pathway

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