Cardiac Fibrosis Alleviated by Exercise Training Is AMPK-Dependent. - Wikidata - wikimedia - TriplyDB

Cardiac Fibrosis Alleviated by Exercise Training Is AMPK-Dependent.

Cardiac Fibrosis Alleviated by Exercise Training Is AMPK-Dependent.

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Exercise for the heart: signaling pathways Asiatic Acid Protects against Cardiac Hypertrophy through Activating AMPKα Signalling Pathway.Adiponectin enhances bone marrow mesenchymal stem cell resistance to flow shear stress through AMP-activated protein kinase signaling Chronic Exercise Training Improved Aortic Endothelial and Mitochondrial Function via an AMPKα2-Dependent Manner Integrative Analysis of PRKAG2 Cardiomyopathy iPS and Microtissue Models Identifies AMPK as a Regulator of Metabolism, Survival, and Fibrosis.Quantitative Biology of Exercise-Induced Signal Transduction Pathways.The Role of MicroRNAs in the Cardiac Response to Exercise.Coupling of myocardial stress resistance and signalling to voluntary activity and inactivity.Resistance exercise improves cardiac function and mitochondrial efficiency in diabetic rat hearts.AMPK and cardiac remodelling.Rosmarinic acid attenuates cardiac fibrosis following long-term pressure overload via AMPKα/Smad3 signaling.Understanding Key Mechanisms of Exercise-Induced Cardiac Protection to Mitigate Disease: Current Knowledge and Emerging Concepts.Melatonin reverses flow shear stress-induced injury in bone marrow mesenchymal stem cells via activation of AMP-activated protein kinase signaling.Exacerbated cardiac fibrosis induced by β-adrenergic activation in old mice due to decreased AMPK activity.

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Cardiac Fibrosis Alleviated by Exercise Training Is AMPK-Dependent.

http://www.wikidata.org/entity/Q35661775

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2015 nî lūn-bûn

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2015年の論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年论文

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2015年论文

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2015年论文

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name

Cardiac Fibrosis Alleviated by Exercise Training Is AMPK-Dependent.

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Cardiac Fibrosis Alleviated by Exercise Training Is AMPK-Dependent.

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Cardiac Fibrosis Alleviated by Exercise Training Is AMPK-Dependent.

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Cardiac Fibrosis Alleviated by Exercise Training Is AMPK-Dependent.

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Cardiac Fibrosis Alleviated by Exercise Training Is AMPK-Dependent.

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Cardiac Fibrosis Alleviated by Exercise Training Is AMPK-Dependent.

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Cardiac Fibrosis Alleviated by Exercise Training Is AMPK-Dependent.

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Han Xiao

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

Jing Shen

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

Qiang Shen

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

Ruifei Chen

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

Xiangbo An

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

Xiaowei Ma

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

Yongnan Fu

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

Youyi Zhang

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

Zijian Li

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

P2860

Role of AMP-activated protein kinase in mechanism of metformin action

Exercise training combined with angiotensin II receptor blockade limits post-infarct ventricular remodelling in rats

Hypoxia induces expression and activation of AMPK in rat dental pulp cells

Targeted disruption of Smad4 in cardiomyocytes results in cardiac hypertrophy and heart failure

Transforming growth factor-beta(1) expression in dilated cardiomyopathy

AMPKalpha2 deletion causes aberrant expression and activation of NAD(P)H oxidase and consequent endothelial dysfunction in vivo: role of 26S proteasomes.

NADPH oxidase 4 (Nox4) is a major source of oxidative stress in the failing heart.

Metformin inhibits P-glycoprotein expression via the NF-κB pathway and CRE transcriptional activity through AMPK activation.

NAD(P)H oxidase 4 mediates transforming growth factor-beta1-induced differentiation of cardiac fibroblasts into myofibroblasts.

Exercise training reduces fibrosis and matrix metalloproteinase dysregulation in the aging rat heart.

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