Cellular mechanisms of diastolic heart failure
- Prosjektnummer
- 2012072
- Ansvarlig person
- William E. Louch
- Institusjon
- Oslo universitetssykehus HF
- Prosjektkategori
- Forskerstipend
- Helsekategori
- Cardiovascular
- Forskningsaktivitet
- 1. Underpinning
NO
Ryanodine receptor dispersion disrupts Ca
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T-tubular collagen: a new player in mechanosensing and disease?
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Increased passive stiffness promotes diastolic dysfunction despite improved Ca2+ handling during left ventricular concentric hypertrophy.
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Impaired left ventricular mechanical and energetic function in mice after cardiomyocyte-specific excision of Serca2.
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Slow Ca²? sparks de-synchronize Ca²? release in failing cardiomyocytes: evidence for altered configuration of Ca²? release units?
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Mind the store: modulating Ca(2+) reuptake with a leaky sarcoplasmic reticulum.
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Beta-adrenergic stimulation maintains cardiac function in Serca2 knockout mice.
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Synchrony of cardiomyocyte Ca(2+) release is controlled by T-tubule organization, SR Ca(2+) content, and ryanodine receptor Ca(2+) sensitivity.
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Integrating multi-scale data to create a virtual physiological mouse heart.
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No rest for the weary: diastolic calcium homeostasis in the normal and failing myocardium.
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Sodium accumulation in SERCA knockout-induced heart failure.
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Extreme sarcoplasmic reticulum volume loss and compensatory T-tubule remodeling after Serca2 knockout.
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Inhibition of SMAD2 phosphorylation preserves cardiac function during pressure overload.
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Secretogranin II; a protein increased in the myocardium and circulation in heart failure with cardioprotective properties.
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Phospholamban ablation in hearts expressing the high affinity SERCA2b isoform normalizes global Ca²? homeostasis but not Ca²?-dependent hypertrophic signaling.
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An analysis of deformation-dependent electromechanical coupling in the mouse heart.
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Strange bedfellows: biologists and mathematical modelers tie the knot on cardiomyocyte calcium homeostasis
Drug Discovery Today, 2014
Slow Ca2+ sparks de-synchronize Ca2+ release in failing cardiomyocytes: evidence for altered configuration of Ca release units?
In press at Journal of Cellular and Molecular Cardiology
Integrating multi-scale data to create a Virtual Physiological Mouse heart
In press at Interface Focus
Beta-adrenergic stimulation maintains cardiac function in Serca2 knockout mice
Conditionally accepted at Biophysical Journal
- Geir Arve Christensen Prosjektdeltaker
- Alessandro Cataliotti Prosjektdeltaker
- Einar Sjaastad Norden Prosjektdeltaker
- Terje R Selnes Kolstad Prosjektdeltaker
- Ornella Manfra Prosjektdeltaker
- Emil Knut Stenersen Espe Prosjektdeltaker
- Marianne Ruud Prosjektdeltaker
- William Edward Louch Prosjektleder
- Xin Shen Prosjektdeltaker
- Åsmund Treu Røe Doktorgradsstipendiat (annen finansiering)
- Ole M Sejersted Prosjektdeltaker
- Ivar Sjaastad Prosjektdeltaker
- Jan Magnus Aronsen Prosjektdeltaker
- Michael Frisk Prosjektdeltaker
- Andrew Gareth Edwards Postdoktorstipendiat
eRapport er utarbeidet av Sølvi Lerfald og Reidar Thorstensen, Regionalt kompetansesenter for klinisk forskning, Helse Vest RHF, og videreutvikles av de fire RHF-ene i fellesskap, med støtte fra Helse Vest IKT
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