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Extracellular SPARC increases cardiomyocyte contraction during health and disease

PloS one, 2019-04, Vol.14 (4), p.e0209534-e0209534

2019

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Selective inhibition of Cx43 hemichannels by Gap19 and its impact on myocardial ischemia/reperfusion injury

Basic research in cardiology, 2013-01, Vol.108 (1), p.309-309, Article 309

2013

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Transcriptome Characterization of Estrogen-Treated Human Myocardium Identifies Myosin Regulatory Light Chain Interacting Protein as a Sex-Specific Element Influencing Contractile Function

Journal of the American College of Cardiology, 2012-01, Vol.59 (4), p.410-417

2012

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Pharmacological Inhibition of Na/Ca Exchange Results in Increased Cellular Ca2 Load Attributable to the Predominance of Forward Mode Block

Circulation research, 2008-06, Vol.102 (11), p.1398-1405

2008

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Intracellular Dyssynchrony of Diastolic Cytosolic [Ca2+] Decay in Ventricular Cardiomyocytes in Cardiac Remodeling and Human Heart Failure

Circulation research, 2013-08, Vol.113 (5), p.527-538

2013

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Targeting Sarcoplasmic Reticulum Ca2+ Uptake to Improve Heart Failure: Hit or Miss

Circulation research, 2010-02, Vol.106 (2), p.230-233

2010

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Exercise training does not improve cardiac function in compensated or decompensated left ventricular hypertrophy induced by aortic stenosis

Journal of molecular and cellular cardiology, 2011-06, Vol.50 (6), p.1017-1025

2011

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Phospholamban ablation in hearts expressing the high affinity SERCA2b isoform normalizes global Ca²⁺ homeostasis but not Ca²⁺-dependent hypertrophic signaling

American journal of physiology. Heart and circulatory physiology, 2012-06, Vol.302 (12), p.H2574-H2582

2012

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ACE-inhibition, but not weight reduction restores cardiomyocyte response to β-adrenergic stimulation in the metabolic syndrome

BMC cardiovascular disorders, 2013-07, Vol.13 (1), p.51-51, Article 51

2013

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Early Exercise Training Normalizes Myofilament Function and Attenuates Left Ventricular Pump Dysfunction in Mice With a Large Myocardial Infarction

Circulation research, 2007-04, Vol.100 (7), p.1079-1088

2007

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Early exercise training after myocardial infarction prevents contractile but not electrical remodelling or hypertrophy

Cardiovascular research, 2010-04, Vol.86 (1), p.72-81

2010

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Cardiac FKBP12.6 overexpression protects against triggered ventricular tachycardia in pressure overloaded mouse hearts

Basic research in cardiology, 2012-03, Vol.107 (2), p.246-246, Article 246

2012

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A SERCA2 pump with an increased Ca2+ affinity can lead to severe cardiac hypertrophy, stress intolerance and reduced life span

Journal of molecular and cellular cardiology, 2006-08, Vol.41 (2), p.308-317

2006

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FKBP12.6 overexpression does not protect against remodelling after myocardial infarction

Experimental physiology, 2013-01, Vol.98 (1), p.134-148

2013

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Sodium Calcium Exchange in the Heart: Necessity or Luxury?

Circulation research, 2004-09, Vol.95 (6), p.549-551

2004

Volltextzugriff (PDF)

Calcium Signaling in Cardiomyocyte Function

Cold Spring Harbor perspectives in biology, 2020-03, Vol.12 (3), p.a035428

2020

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Increased phospholamban phosphorylation limits the force–frequency response in the MLP –/– mouse with heart failure

Journal of molecular and cellular cardiology, 2006-03, Vol.40 (3), p.350-360

2006

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Ventricular Phosphodiesterase-5 Expression Is Increased in Patients With Advanced Heart Failure and Contributes to Adverse Ventricular Remodeling After Myocardial Infarction in Mice

Circulation (New York, N.Y.), 2009-01, Vol.119 (3), p.408-416

2009

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Melusin protects from cardiac rupture and improves functional remodelling after myocardial infarction

Cardiovascular research, 2014-01, Vol.101 (1), p.97-107

2014

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Mechanisms underlying the frequency dependence of contraction and [Ca(2+)](i) transients in mouse ventricular myocytes

The Journal of physiology, 2002-09, Vol.543 (Pt 3), p.889-898

2002

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Characterizing the trigger for sarcoplasmic reticulum Ca2+ release in cardiac myocytes

Cold Spring Harbor protocols, 2015-04, Vol.2015 (4), p.398

2015

Volltextzugriff (PDF)

Inactivation of Smad5 in Endothelial Cells and Smooth Muscle Cells Demonstrates that Smad5 Is Required for Cardiac Homeostasis

The American journal of pathology, 2007-05, Vol.170 (5), p.1460-1472

2007

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Spatial and Temporal Inhomogeneities During Ca2+ Release From the Sarcoplasmic Reticulum in Pig Ventricular Myocytes

Circulation research, 2002-11, Vol.91 (11), p.1023-1030

2002

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Replacement of the muscle-specific sarcoplasmic reticulum Ca(2+)-ATPase isoform SERCA2a by the nonmuscle SERCA2b homologue causes mild concentric hypertrophy and impairs contraction-relaxation of the heart

Circulation research, 2001-10, Vol.89 (9), p.838-846

2001

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Ca2+ transport ATPase isoforms SERCA2a and SERCA2b are targeted to the same sites in the murine heart

Cell calcium (Edinburgh), 2003-12, Vol.34 (6), p.457-464

2003

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Extracellular SPARC increases cardiomyocyte contraction during health and disease

Selective inhibition of Cx43 hemichannels by Gap19 and its impact on myocardial ischemia/reperfusion injury

Transcriptome Characterization of Estrogen-Treated Human Myocardium Identifies Myosin Regulatory Light Chain Interacting Protein as a Sex-Specific Element Influencing Contractile Function

Pharmacological Inhibition of Na/Ca Exchange Results in Increased Cellular Ca2 Load Attributable to the Predominance of Forward Mode Block

Intracellular Dyssynchrony of Diastolic Cytosolic [Ca2+] Decay in Ventricular Cardiomyocytes in Cardiac Remodeling and Human Heart Failure

Targeting Sarcoplasmic Reticulum Ca2+ Uptake to Improve Heart Failure: Hit or Miss

Exercise training does not improve cardiac function in compensated or decompensated left ventricular hypertrophy induced by aortic stenosis

Phospholamban ablation in hearts expressing the high affinity SERCA2b isoform normalizes global Ca²⁺ homeostasis but not Ca²⁺-dependent hypertrophic signaling

ACE-inhibition, but not weight reduction restores cardiomyocyte response to β-adrenergic stimulation in the metabolic syndrome

Early Exercise Training Normalizes Myofilament Function and Attenuates Left Ventricular Pump Dysfunction in Mice With a Large Myocardial Infarction

Early exercise training after myocardial infarction prevents contractile but not electrical remodelling or hypertrophy

Cardiac FKBP12.6 overexpression protects against triggered ventricular tachycardia in pressure overloaded mouse hearts

A SERCA2 pump with an increased Ca2+ affinity can lead to severe cardiac hypertrophy, stress intolerance and reduced life span

FKBP12.6 overexpression does not protect against remodelling after myocardial infarction

Sodium Calcium Exchange in the Heart: Necessity or Luxury?

Calcium Signaling in Cardiomyocyte Function

Increased phospholamban phosphorylation limits the force–frequency response in the MLP –/– mouse with heart failure

Ventricular Phosphodiesterase-5 Expression Is Increased in Patients With Advanced Heart Failure and Contributes to Adverse Ventricular Remodeling After Myocardial Infarction in Mice

Melusin protects from cardiac rupture and improves functional remodelling after myocardial infarction

Mechanisms underlying the frequency dependence of contraction and [Ca(2+)](i) transients in mouse ventricular myocytes

Characterizing the trigger for sarcoplasmic reticulum Ca2+ release in cardiac myocytes

Inactivation of Smad5 in Endothelial Cells and Smooth Muscle Cells Demonstrates that Smad5 Is Required for Cardiac Homeostasis

Spatial and Temporal Inhomogeneities During Ca2+ Release From the Sarcoplasmic Reticulum in Pig Ventricular Myocytes

Replacement of the muscle-specific sarcoplasmic reticulum Ca(2+)-ATPase isoform SERCA2a by the nonmuscle SERCA2b homologue causes mild concentric hypertrophy and impairs contraction-relaxation of the heart

Ca2+ transport ATPase isoforms SERCA2a and SERCA2b are targeted to the same sites in the murine heart

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