Deletion of Fn14 receptor protects from right heart fibrosis and dysfunction - Wikidata - wikimedia - TriplyDB

Deletion of Fn14 receptor protects from right heart fibrosis and dysfunction

Deletion of Fn14 receptor protects from right heart fibrosis and dysfunction

http://www.wikidata.org/entity/Q36683886

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5-HT2B receptor antagonists inhibit fibrosis and protect from RV heart failure The TWEAK-Fn14 pathway: a potent regulator of skeletal muscle biology in health and disease Repair Injured Heart by Regulating Cardiac Regenerative Signals Interaction of TWEAK with Fn14 leads to the progression of fibrotic liver disease by directly modulating hepatic stellate cell proliferation The TWEAK-Fn14 dyad is involved in age-associated pathological changes in skeletal muscle Hepatocyte growth factor regulates the TGF-β1-induced proliferation, differentiation and secretory function of cardiac fibroblasts.Role of Fn14 in acute alcoholic steatohepatitis in mice.Fn14, a Downstream Target of the TGF-β Signaling Pathway, Regulates Fibroblast Activation.Heightened TWEAK-NF-κB signaling and inflammation-associated fibrosis in paralyzed muscles of men with chronic spinal cord injury.Achievement of a target dose of bisoprolol may not be a preferred option for attenuating pressure overload-induced cardiac hypertrophy and fibrosis Contributions of cardiomyocyte-cardiac fibroblast-immune cell interactions in heart failure development.The TWEAK-Fn14 system as a potential drug target.Investigational drugs targeting cardiac fibrosis.TWEAK-Fn14 Cytokine-Receptor Axis: A New Player of Myocardial Remodeling and Cardiac Failure The role of liver progenitor cells during liver regeneration, fibrogenesis, and carcinogenesis.p38 MAPK Inhibition Improves Heart Function in Pressure Loaded Right Ventricular Hypertrophy.TWEAK protects cardiomyocyte against apoptosis in a PI3K/AKT pathway dependent manner Fn14 promotes differentiation of human mesenchymal stem cells into heart valvular interstitial cells by phenotypic characterization.Maintained right ventricular pressure overload induces ventricular-arterial decoupling in mice.Role of Omentin, Vaspin, Cardiotrophin-1, TWEAK and NOV/CCN3 in Obesity and Diabetes Development TWEAK and NT-proBNP levels predict exercise capacity in hypertrophic cardiomyopathy.Is p38 MAPK a Dark Force in Right Ventricular Hypertrophy and Failure in Pulmonary Arterial Hypertension?TWEAK promotes migration and invasion in MEFs through a mechanism dependent on ERKs activation and Fibulin 3 down-regulation.Tweak up-regulates endothelin-1 system in mouse and human endothelial cells.Cardioprotective effects of early and late aerobic exercise training in experimental pulmonary arterial hypertension.Effect of Riociguat and Sildenafil on Right Heart Remodeling and Function in Pressure Overload Induced Model of Pulmonary Arterial Banding.Tnfrsf12a-Mediated Atherosclerosis Signaling and Inflammatory Response as a Common Protection Mechanism of Shuxuening Injection Against Both Myocardial and Cerebral Ischemia-Reperfusion Injuries.Inflammatory Mediators Drive Adverse Right Ventricular Remodeling and Dysfunction and Serve as Potential Biomarkers.

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Deletion of Fn14 receptor protects from right heart fibrosis and dysfunction

http://www.wikidata.org/entity/Q36683886

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2013 nî lūn-bûn

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2013年の論文

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2013年論文

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2013年論文

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2013年論文

@zh-hk

2013年論文

@zh-mo

2013年論文

@zh-tw

2013年论文

@wuu

2013年论文

@zh

2013年论文

@zh-cn

name

Deletion of Fn14 receptor protects from right heart fibrosis and dysfunction

@ast

Deletion of Fn14 receptor protects from right heart fibrosis and dysfunction

@en

type

label

Deletion of Fn14 receptor protects from right heart fibrosis and dysfunction

@ast

Deletion of Fn14 receptor protects from right heart fibrosis and dysfunction

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prefLabel

Deletion of Fn14 receptor protects from right heart fibrosis and dysfunction

@ast

Deletion of Fn14 receptor protects from right heart fibrosis and dysfunction

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Basic Research in Cardiology

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Deletion of Fn14 receptor protects from right heart fibrosis and dysfunction

@en

P2093

Astrid Wietelmann

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

Chinmoy Patra

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

Felix B Engel

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

Frederic Strobl

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

Guido Posern

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

Jakub M Swiercz

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

Ralph T Schermuly

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

Tatyana Novoyatleva

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

Timothy S Zheng

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

Wiebke Janssen

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

P2860

Potentiation of serum response factor activity by a family of myocardin-related transcription factors.

Modulation of adverse cardiac remodeling by STARS, a mediator of MEF2 signaling and SRF activity

TWEAK induces angiogenesis and proliferation of endothelial cells

Actin dynamics control SRF activity by regulation of its coactivator MAL

A novel role for tumor necrosis factor-like weak inducer of apoptosis (TWEAK) in the development of cardiac dysfunction and failure.

TWEAK/Fn14 pathway: an immunological switch for shaping tissue responses.

TWEAK induces liver progenitor cell proliferation

Reversal of experimental pulmonary hypertension by PDGF inhibition.

Myocardin-related transcription factor-a controls myofibroblast activation and fibrosis in response to myocardial infarction.

Association of left atrial endothelin-1 with atrial rhythm, size, and fibrosis in patients with structural heart disease.

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2013-01-17T00:00:00Z

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