CaMKII inhibition in heart failure, beneficial, harmful, or both - Wikidata - awgldk - TriplyDB

CaMKII inhibition in heart failure, beneficial, harmful, or both

CaMKII inhibition in heart failure, beneficial, harmful, or both

http://www.wikidata.org/entity/Q35900927

about

Toward a hierarchy of mechanisms in CaMKII-mediated arrhythmia.Atrial remodelling in atrial fibrillation: CaMKII as a nodal proarrhythmic signal Posttranslational modifications of cardiac ryanodine receptors: Ca(2+) signaling and EC-coupling.Molecular targets of current and prospective heart failure therapies.Transient outward potassium channel: a heart failure mediator.Loss of myocardial retinoic acid receptor α induces diastolic dysfunction by promoting intracellular oxidative stress and calcium mishandling in adult mice.Stretch current-induced abnormal impulses in CaMKIIδ knockout mouse ventricular myocytes Calmodulin/CaMKII inhibition improves intercellular communication and impulse propagation in the heart and is antiarrhythmic under conditions when fibrosis is absent.CaMKII-dependent myofilament Ca2+ desensitization contributes to the frequency-dependent acceleration of relaxation.Integrin-linked kinase mediates force transduction in cardiomyocytes by modulating SERCA2a/PLN function.Assessment of Sarcoplasmic Reticulum Calcium Reserve and Intracellular Diastolic Calcium Removal in Isolated Ventricular Cardiomyocytes.Vitexin protects against cardiac hypertrophy via inhibiting calcineurin and CaMKII signaling pathways.The Rho kinase inhibitor, fasudil, ameliorates diabetes-induced cardiac dysfunction by improving calcium clearance and actin remodeling.CaMKII: do not work too hard in the failing heart.Inhibition of calcium/calmodulin-dependent kinase II restores contraction and relaxation in isolated cardiac muscle from type 2 diabetic rats.

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CaMKII inhibition in heart failure, beneficial, harmful, or both

http://www.wikidata.org/entity/Q35900927

description

2012 nî lūn-bûn

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2012年の論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

@zh-mo

2012年論文

@zh-tw

2012年论文

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2012年论文

@zh

2012年论文

@zh-cn

name

CaMKII inhibition in heart failure, beneficial, harmful, or both

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CaMKII inhibition in heart failure, beneficial, harmful, or both

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type

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CaMKII inhibition in heart failure, beneficial, harmful, or both

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CaMKII inhibition in heart failure, beneficial, harmful, or both

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CaMKII inhibition in heart failure, beneficial, harmful, or both

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CaMKII inhibition in heart failure, beneficial, harmful, or both

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AJPHEART.00812.2011

P1433

American Journal of Physiology - Heart and Circulatory Physiology

P1476

CaMKII inhibition in heart failure, beneficial, harmful, or both

@en

P2093

Arnaud Guilbert

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

Dongwu Lai

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

Hyun Joung Lim

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

Jun Cheng

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

Lin Xu

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

Thitima Keskanokwong

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

Yanggan Wang

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

P2860

The deltaC isoform of CaMKII is activated in cardiac hypertrophy and induces dilated cardiomyopathy and heart failure

CaMKII tethers to L-type Ca2+ channels, establishing a local and dedicated integrator of Ca2+ signals for facilitation

Differential activation of stress-response signaling in load-induced cardiac hypertrophy and failure.

Calmodulin kinase signaling in heart: an intriguing candidate target for therapy of myocardial dysfunction and arrhythmias.

Remodeling of early-phase repolarization: a mechanism of abnormal impulse conduction in heart failure

Autonomic aspects of arrhythmogenesis: the enduring and the new.

Involvement of extracellular signal-regulated kinases 1/2 in cardiac hypertrophy and cell death.

Calmodulin kinase and L-type calcium channels; a recipe for arrhythmias?

Role of Ca2+/calmodulin-dependent protein kinase II in cardiac hypertrophy and heart failure.

Tissue Doppler imaging a new prognosticator for cardiovascular diseases.

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10.1152/AJPHEART.00812.2011

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7

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302

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221789190

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22287581

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3330794

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