<i>Retracted</i>: Emodin protects H9c2 cells against hypoxia‐induced injury via regulation of miR‐26a/survivin and the JAK1/STAT3 pathway

Huang, Jiancheng; Li, Xiaobing; Liu, Pujuan; Wang, Jun; Li, Hongying

doi:10.1002/jcb.28385

Cited by 3 publications

(7 citation statements)

References 35 publications

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Section: Targets and Studies Of Emodin Against Anti-cardiovascular DImentioning

confidence: 93%

“…Emodin treatment in H9c2 cells with myocarditis Anti-apoptosis (Liu et al, 2013) caspase-3↓, Bcl-2↑ Emodin treatment in BALB/c mice and HEp-2 cells with viral myocarditis (Zhang et al, 2019) miR-138↑, MLK3↓, p53 and p21↓, cyclin D1↑, caspase-3 and caspase-9↓Sirt1/AKT, and Wnt/b-catenin pathways activated, Emodin treatment in H9c2 cells with myocardial ischemia (Huang et al, 2019) miR-26a↓, survivin↑, caspase-3, and caspase-9↓, JAK1/STAT3 signal activated Emodin treatment in H9c2 cells with myocardial ischemia (Ye et al, 2019) GSDMD-N↓, IL-1b↓, TLR4/MyD88/NF-kB/NLRP3 inhibited Emodin treatment in Sprague-Dawley rats cardiomyocytes with ischemia/reperfusion injury Anti-myocardial fibrosis (Xiao et al, 2019) MTA3↑, COL1A2, and a-SMA↓ Emodin treatment in mouse model of pathological cardiac hypertrophy with excess fibrosis Anti-cardiac hypertrophy (Evans et al, 2020) I HDAC and II HDAC activity inhibited, histone acetylation in cardiomyocytes↑, ERK phosphorylation inhibited Emodin treatment in C57BL/6 mice with cardiac hypertrophy (transverse aortic constriction-induced) and fibrosis (AngII-induced) (Gao et al, 2020) SIRT3↑, modulation of mitochondrial SIRT3 and its downstream signaling pathway…”

Section: References Finding Methodologymentioning

confidence: 99%

“…Furthermore, survival rate of mice or cells was improved, MTD was prolonged, and HW/BW, viral titer and myocardial pathological score caused by viral infection were decreased. Studies (Huang et al, 2019;Zhang et al, 2019) also showed that H9c2 cells with myocardial ischemia (hypoxiainduced) after treatment with emodin (15 mM or 20 mM) had the effect of down-regulating caspase-3 and caspase-9. Regarding the role of emodin, Leung et al (2020) also reported that emodin can regulate the kinase (ERK)-1/2 signaling pathway in vivo and in vitro by activating extracellular signaling, increasing the expression of Bcl-2 and glutamate transporter-1 (GLT-l), and inhibiting the activated level of caspase-3.…”

Section: Anti-apoptosismentioning

confidence: 97%

“…In addition, the relationship between hypoxic treatment and survivin expression has also been found in previous studies ( Zhu et al., 2001 ; Zhang et al., 2007 ). Huang et al. (2019) revealed that hypoxia decreased the accumulated level of survivin while emodin enhanced the expression of survivin, which provided a reason for emodin to inhibit cell apoptosis due to the anti-apoptosis effects of survival.…”

Section: Targets and Studies Of Emodin Against Anti-cardiovascular DImentioning

confidence: 99%

“…MiR-26a plays a crucial role in the regulation of cardiomyocytes ( Liu et al., 2016 ). Huang et al found that the up-regulation of miR-26a promoted the apoptosis of hypoxia-treated H9c2 cells, while emodin (15 and 20 μM) could negatively regulate the expression of miR-26a and reduce the apoptosis by regulating miR-26a ( Huang et al., 2019 ). Meanwhile, survivin is a member of the inhibitor of apoptosis protein (IAPs) family.…”

Section: Targets and Studies Of Emodin Against Anti-cardiovascular DImentioning

confidence: 99%

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Molecular Mechanisms of Action of Emodin: As an Anti-Cardiovascular Disease Drug

Gao

Pang

et al. 2020

Front. Pharmacol.

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Emodin is a natural occurring anthraquinone derivative isolated from roots and barks of numerous plants, molds, and lichens. It is found to be an active ingredient in different Chinese herbs including Rheum palmatum and Polygonam multiflorum, and it is a pleiotropic molecule with diuretic, vasorelaxant, anti-bacterial, anti-viral, antiulcerogenic, anti-inflammatory, and anti-cancer effects. Moreover, emodin has also been shown to have a wide activity of anti-cardiovascular diseases. It is mainly involved in multiple molecular targets such as inflammatory, anti-apoptosis, anti-hypertrophy, antifibrosis, anti-oxidative damage, abnormal, and excessive proliferation of smooth muscle cells in cardiovascular diseases. As a new type of cardiovascular disease treatment drug, emodin has broad application prospects. However, a large amount of evidences detailing the effect of emodin on many signaling pathways and cellular functions in cardiovascular disease, the overall understanding of its mechanisms of action remains elusive. In addition, by describing the evidence of the effects of emodin in detail, the toxicity and poor oral bioavailability of mice have been continuously discovered. This review aims to describe a timely overview of emodin related to the treatment of cardiovascular disease. The emphasis is to summarize the pharmacological effects of emodin as an anticardiovascular drug, as well as the targets and its potential mechanisms. Furthermore, the treatment of emodin compared with conventional cardiovascular drugs or target inhibitors, the toxicity, pharmacokinetics and derivatives of emodin were discussed.

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Section: Targets and Studies Of Emodin Against Anti-cardiovascular DImentioning

confidence: 93%

Section: References Finding Methodologymentioning

confidence: 99%

Section: Anti-apoptosismentioning

confidence: 97%

Section: Targets and Studies Of Emodin Against Anti-cardiovascular DImentioning

confidence: 99%

Section: Targets and Studies Of Emodin Against Anti-cardiovascular DImentioning

confidence: 99%

See 3 more Smart Citations

Molecular Mechanisms of Action of Emodin: As an Anti-Cardiovascular Disease Drug

Gao

Pang

et al. 2020

Front. Pharmacol.

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Kanglexin, a novel anthraquinone compound, protects against myocardial ischemic injury in mice by suppressing NLRP3 and pyroptosis

Bian

Pang

et al. 2019

Acta Pharmacol Sin

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Pyroptosis is a form of inflammatory cell death that could be driven by the nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome activation following myocardial infarction (MI). Emerging evidence suggests the therapeutic potential for ameliorating MI-induced myocardial damages by targeting NLRP3 and pyroptosis. In this study, we investigated the myocardial protection effect of a novel anthraquinone compound (4,5-dihydroxy-7-methyl-9,10-anthraquinone-2-ethyl succinate) named Kanglexin (KLX) in vivo and in vitro. Male C57BL/6 mice were pre-treated either with KLX (20, 40 mg· kg −1 per day, intragastric gavage) or vehicle for 7 consecutive days prior to ligation of coronary artery to induce permanent MI. KLX administration dose-dependently reduced myocardial infarct size and lactate dehydrogenase release and improved cardiac function as compared to vehicle-treated mice 24 h after MI. We found that MI triggered NLRP3 inflammasome activation leading to conversion of interleukin-1β (IL-1β) and IL-18 into their active mature forms in the heart, which could expand the infarct size and drive cardiac dysfunction. We also showed that MI induced pyroptosis, as evidenced by increased DNA fragmentation, mitochondrial swelling, and cell membrane rupture, as well as increased levels of pyroptosis-related proteins, including gasdermin D, N-terminal GSDMD, and cleaved caspase-1. All these detrimental alterations were prevented by KLX. In hypoxia- or lipopolysaccharide (LPS)-treated neonatal mouse ventricular cardiomyocytes, we showed that KLX (10 μM) decreased the elevated levels of terminal deoxynucleotidyl transferase dUTP nick end labeling- and propidium iodide-positive cells, and pyroptosis-related proteins. We conclude that KLX prevents MI-induced cardiac damages and cardiac dysfunction at least partly through attenuating NLRP3 and subsequent cardiomyocyte pyroptosis, and it is worthy of more rigorous investigations for its potential for alleviating ischemic heart disease.

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Identification of Potential miRNA-mRNA Regulatory Network in Tetralogy of Fallot: A Network Biology Approach

Wang

Lyu

et al. 2021

Preprint

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BackgroundTetralogy of Fallot (ToF) is one of the most prevalent and fatal birth defects. Its pathogenesis remains unknown and it’s not easily diagnosed at early stage. Therefore, it’s necessary to explore the critical regulators and molecular mechanism in ToF to find out novel molecular markers for early diagnosis.MethodsThree ToF datasets (GSE35490, GSE40128, GSE36761) were downloaded from the GEO database. The differentially expressed microRNAs (DEMs) and mRNAs (DEGs) were identified between ToF infants and normal infants after data preprocessing, followed by GO and KEGG analysis of DEGs. Then, PPI network and modular analysis were performed to identify the hub genes. Ultimately, potential miRNA-mRNA pathways in ToF were constructed based on the integrated data.Results22 overlapping DEMs were found in the GES35490 and GSE40128. Simultaneous, 181 intersected genes were found and identified as the significant DEGs including 84 down-regulated DEGs and 97 up-regulated DEGs. Further, 20 hub genes ranked by top 10% with high connectivity, including STAT3, FBN1, RUNX2, were found by PPT network and modular analysis. Furthermore, GO and KEGG analysis showed these DEGs were linked to cell cycle, apoptotic process, transcription activity and FOX signaling pathway. Additionally, we establish three potential miRNA-mRNA pathway, including miR-22-STAT3, miR-336/miR486-FBN1, miR-222-RUNX2, which can participate in the formation of ToF by cell cycle and transcription activity.ConclusionsThree miRNA-mRNA pathways were established and indicated cell cycle and transcription activity may be involved in the pathogenesis of ToF. Our study provided a novel bio-marker for early diagnosis of ToF.

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Retracted: Emodin protects H9c2 cells against hypoxia‐induced injury via regulation of miR‐26a/survivin and the JAK1/STAT3 pathway

Cited by 3 publications

References 35 publications

Molecular Mechanisms of Action of Emodin: As an Anti-Cardiovascular Disease Drug

Molecular Mechanisms of Action of Emodin: As an Anti-Cardiovascular Disease Drug

Kanglexin, a novel anthraquinone compound, protects against myocardial ischemic injury in mice by suppressing NLRP3 and pyroptosis

Identification of Potential miRNA-mRNA Regulatory Network in Tetralogy of Fallot: A Network Biology Approach

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