Cardiac fibroblast glycogen synthase kinase-3β regulates ventricular remodeling and dysfunction in ischemic heart. - Wikidata - awgldk - TriplyDB

Cardiac fibroblast glycogen synthase kinase-3β regulates ventricular remodeling and dysfunction in ischemic heart.

Cardiac fibroblast glycogen synthase kinase-3β regulates ventricular remodeling and dysfunction in ischemic heart.

http://www.wikidata.org/entity/Q42859300

about

The GSK-3 family as therapeutic target for myocardial diseases Hypothyroidism and its rapid correction alter cardiac remodeling Genetic tools for identifying and manipulating fibroblasts in the mouse Natural product derivative BIO promotes recovery after myocardial infarction via unique modulation of the cardiac microenvironment Ablation of periostin inhibits post-infarction myocardial regeneration in neonatal mice mediated by the phosphatidylinositol 3 kinase/glycogen synthase kinase 3β/cyclin D1 signalling pathway.Piperine Attenuates Pathological Cardiac Fibrosis Via PPAR-γ/AKT Pathways.Regulation of transforming growth factor-beta1 (TGF-β1)-induced pro-fibrotic activities by circadian clock gene BMAL1.Fibroblast deletion of ROCK2 attenuates cardiac hypertrophy, fibrosis, and diastolic dysfunction Exendin-4 protects against post-myocardial infarction remodelling via specific actions on inflammation and the extracellular matrix DIM attenuates TGF-β1-induced myofibroblast differentiation in neonatal rat cardiac fibroblasts.Glycogen synthase kinase-3 inhibition attenuates fibroblast activation and development of fibrosis following renal ischemia-reperfusion in mice.Luteolin alleviates post-infarction cardiac dysfunction by up-regulating autophagy through Mst1 inhibition Central role for GSK3β in the pathogenesis of arrhythmogenic cardiomyopathy.Inhibition of glycogen synthase kinase-3β prevents sympathetic hyperinnervation in infarcted rats.Atrial remodeling, fibrosis, and atrial fibrillation.Mechanoregulation of cardiac myofibroblast differentiation: implications for cardiac fibrosis and therapy.The role of mid-chain hydroxyeicosatetraenoic acids in the pathogenesis of hypertension and cardiac hypertrophy.Modeling the Human Scarred Heart In Vitro: Toward New Tissue Engineered Models.Myocardial apoptosis in heart disease: does the emperor have clothes?Molecular networks underlying myofibroblast fate and fibrosis.Transforming growth factor-β-dependent Wnt secretion controls myofibroblast formation and myocardial fibrosis progression in experimental autoimmune myocarditis.Cardiac Fibroblast GRK2 Deletion Enhances Contractility and Remodeling Following Ischemia/Reperfusion Injury.Loss of Adult Cardiac Myocyte GSK-3 Leads to Mitotic Catastrophe Resulting in Fatal Dilated Cardiomyopathy.Transforming growth factor β: A potential biomarker and therapeutic target of ventricular remodeling.CTRP3 attenuates post-infarct cardiac fibrosis by targeting Smad3 activation and inhibiting myofibroblast differentiation.Kinase inhibitor screening using artificial neural networks and engineered cardiac biowires Calreticulin Is Required for TGF-β-Induced Epithelial-to-Mesenchymal Transition during Cardiogenesis in Mouse Embryonic Stem Cells.Response by Zhou et al to Letter Regarding Article, "Loss of Adult Cardiac Myocyte GSK-3 Leads to Mitotic Catastrophe Resulting in Fatal Dilated Cardiomyopathy".The role of α-smooth muscle actin in fibroblast-mediated matrix contraction and remodeling.Opposing Actions of Fibroblast and Cardiomyocyte Smad3 Signaling in the Infarcted Myocardium.2,5-Dimethylcelecoxib prevents pressure-induced left ventricular remodeling through GSK-3 activation.Cardiomyocyte-specific deletion of GSK-3β leads to cardiac dysfunction in a diet induced obesity model.Rosmarinic acid attenuates cardiac fibrosis following long-term pressure overload via AMPKα/Smad3 signaling.Hypoxia-stimulated cardiac fibroblast production of IL-6 promotes myocardial fibrosis via the TGF-β1 signaling pathway.Galectin-3 in Atrial Fibrillation: Mechanisms and Therapeutic Implications.Glycogen synthase kinase 3β inhibition reduces mitochondrial oxidative stress in chronic myocardial ischemia.Entanglement of GSK-3β, β-catenin and TGF-β1 signaling network to regulate myocardial fibrosis.MicroRNA-21 prevents excessive inflammation and cardiac dysfunction after myocardial infarction through targeting KBTBD7.Cardiac fibrosis: new insights into the pathogenesis

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Cardiac fibroblast glycogen synthase kinase-3β regulates ventricular remodeling and dysfunction in ischemic heart.

http://www.wikidata.org/entity/Q42859300

description

2014 nî lūn-bûn

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2014年の論文

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2014年論文

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2014年論文

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2014年論文

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2014年論文

@zh-mo

2014年論文

@zh-tw

2014年论文

@wuu

2014年论文

@zh

2014年论文

@zh-cn

name

Cardiac fibroblast glycogen sy ...... dysfunction in ischemic heart.

@en

Cardiac fibroblast glycogen sy ...... dysfunction in ischemic heart.

@nl

type

label

Cardiac fibroblast glycogen sy ...... dysfunction in ischemic heart.

@en

Cardiac fibroblast glycogen sy ...... dysfunction in ischemic heart.

@nl

prefLabel

Cardiac fibroblast glycogen sy ...... dysfunction in ischemic heart.

@en

Cardiac fibroblast glycogen sy ...... dysfunction in ischemic heart.

@nl

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CIRCULATIONAHA.113.008364

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Cardiac fibroblast glycogen sy ...... dysfunction in ischemic heart.

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Daohai Yu

http://www.w3.org/2001/XMLSchema#string

Emily J Tsai

http://www.w3.org/2001/XMLSchema#string

Erhe Gao

http://www.w3.org/2001/XMLSchema#string

Jibin Zhou

http://www.w3.org/2001/XMLSchema#string

Justine E Yu

http://www.w3.org/2001/XMLSchema#string

Ronald J Vagnozzi

http://www.w3.org/2001/XMLSchema#string

Yuanjun Guo

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P2860

TGFβ signalling in context

Endothelial-to-mesenchymal transition contributes to cardiac fibrosis

Cardiac fibroblast: the renaissance cell.

Cardiac fibroblasts are essential for the adaptive response of the murine heart to pressure overload.

Glycogen synthase kinase-3beta regulates post-myocardial infarction remodeling and stress-induced cardiomyocyte proliferation in vivo

Wnt1/βcatenin injury response activates the epicardium and cardiac fibroblasts to promote cardiac repair.

Deficiency of biglycan causes cardiac fibroblasts to differentiate into a myofibroblast phenotype.

Constitutive Smad linker phosphorylation in melanoma: a mechanism of resistance to transforming growth factor-β-mediated growth inhibition.

Mechanism and regulation of nucleocytoplasmic trafficking of smad.

Deletion of periostin reduces muscular dystrophy and fibrosis in mice by modulating the transforming growth factor-β pathway.

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419-430

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5

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130

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James R. Woodgett

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2014-06-04T00:00:00Z

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262884828

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4153405

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