Published in Circ Heart Fail on May 19, 2014
Cardiac Non-myocyte Cells Show Enhanced Pharmacological Function Suggestive of Contractile Maturity in Stem Cell Derived Cardiomyocyte Microtissues. Toxicol Sci (2016) 0.78
Pathophysiological mechanism and therapeutic role of S100 proteins in cardiac failure: a systematic review. Heart Fail Rev (2016) 0.75
Left ventricular assist device and drug therapy for the reversal of heart failure. N Engl J Med (2006) 8.98
Decreased catecholamine sensitivity and beta-adrenergic-receptor density in failing human hearts. N Engl J Med (1982) 6.79
Myocyte recovery after mechanical circulatory support in humans with end-stage heart failure. Circulation (1998) 3.41
Reversal of severe heart failure with a continuous-flow left ventricular assist device and pharmacological therapy: a prospective study. Circulation (2011) 3.18
Calcium upregulation by percutaneous administration of gene therapy in cardiac disease (CUPID Trial), a first-in-human phase 1/2 clinical trial. J Card Fail (2009) 2.89
Relation between myocardial function and expression of sarcoplasmic reticulum Ca(2+)-ATPase in failing and nonfailing human myocardium. Circ Res (1994) 2.82
Cardiac improvement during mechanical circulatory support: a prospective multicenter study of the LVAD Working Group. Circulation (2007) 2.34
Effects of continuous-flow versus pulsatile-flow left ventricular assist devices on myocardial unloading and remodeling. Circ Heart Fail (2011) 2.19
Differential gene expression and genomic patient stratification following left ventricular assist device support. J Am Coll Cardiol (2003) 2.08
Is bridge to recovery more likely with pulsatile left ventricular assist devices than with nonpulsatile-flow systems? Ann Thorac Surg (2011) 1.94
Is depressed myocyte contractility centrally involved in heart failure? Circ Res (2003) 1.88
Gene therapy in heart failure. Circ Res (2008) 1.79
Improved left ventricular function after chronic left ventricular unloading. Ann Thorac Surg (1996) 1.74
Stable myocardial-specific AAV6-S100A1 gene therapy results in chronic functional heart failure rescue. Circulation (2007) 1.73
Clinical, molecular, and genomic changes in response to a left ventricular assist device. J Am Coll Cardiol (2011) 1.69
S100A1 genetically targeted therapy reverses dysfunction of human failing cardiomyocytes. J Am Coll Cardiol (2011) 1.68
Cellular and hemodynamics responses of failing myocardium to continuous flow mechanical circulatory support using the DeBakey-Noon left ventricular assist device: a comparative analysis with pulsatile-type devices. J Heart Lung Transplant (2005) 1.64
Incomplete recovery of myocyte contractile function despite improvement of myocardial architecture with left ventricular assist device support. Circ Heart Fail (2011) 1.64
Cardiac S100A1 protein levels determine contractile performance and propensity toward heart failure after myocardial infarction. Circulation (2006) 1.64
Cardiac adenoviral S100A1 gene delivery rescues failing myocardium. J Clin Invest (2004) 1.58
Reverse remodeling in heart failure--mechanisms and therapeutic opportunities. Nat Rev Cardiol (2011) 1.49
Impaired cardiac contractility response to hemodynamic stress in S100A1-deficient mice. Mol Cell Biol (2002) 1.43
Transgenic overexpression of the Ca2+-binding protein S100A1 in the heart leads to increased in vivo myocardial contractile performance. J Biol Chem (2003) 1.43
S100A1: a regulator of myocardial contractility. Proc Natl Acad Sci U S A (2001) 1.42
Gender influences on sarcoplasmic reticulum Ca2+-handling in failing human myocardium. J Mol Cell Cardiol (2001) 1.40
Chronic unloading by left ventricular assist device reverses contractile dysfunction and alters gene expression in end-stage heart failure. Circulation (2000) 1.32
Impact of left ventricular assist device (LVAD) support on the cardiac reverse remodeling process. Prog Biophys Mol Biol (2008) 1.30
Altered expression of the Ca(2+)-binding protein S100A1 in human cardiomyopathy. Biochim Biophys Acta (1996) 1.29
LVAD-induced reverse remodeling: basic and clinical implications for myocardial recovery. J Card Fail (2006) 1.28
Mechanisms of disease: ion channel remodeling in the failing ventricle. Nat Clin Pract Cardiovasc Med (2008) 1.24
Ca2+ cycling and new therapeutic approaches for heart failure. Circulation (2010) 1.16
Left ventricular assist device support normalizes left and right ventricular beta-adrenergic pathway properties. J Am Coll Cardiol (2005) 1.13
Mechanical unloading leads to echocardiographic, electrocardiographic, neurohormonal, and histologic recovery. J Heart Lung Transplant (2005) 1.10
Inotropic effects of angiotensin II on human cardiac muscle in vitro. Circulation (1990) 1.10
S100A1: a novel inotropic regulator of cardiac performance. Transition from molecular physiology to pathophysiological relevance. Am J Physiol Regul Integr Comp Physiol (2007) 1.08
S100A1 decreases calcium spark frequency and alters their spatial characteristics in permeabilized adult ventricular cardiomyocytes. Cell Calcium (2006) 1.07
Effects of pulsatile- and continuous-flow left ventricular assist devices on left ventricular unloading. J Heart Lung Transplant (2008) 1.04
Reversing advanced heart failure by targeting Ca2+ cycling. Annu Rev Med (2008) 1.01
S100A1 gene therapy preserves in vivo cardiac function after myocardial infarction. Mol Ther (2005) 1.01
The small EF-hand Ca2+ binding protein S100A1 increases contractility and Ca2+ cycling in rat cardiac myocytes. Basic Res Cardiol (2002) 1.01
Myocardial gene expression of regulators of myocyte apoptosis and myocyte calcium homeostasis during hemodynamic unloading by ventricular assist devices in patients with end-stage heart failure. Circulation (1999) 1.01
Right ventricular upregulation of the Ca(2+) binding protein S100A1 in chronic pulmonary hypertension. Biochim Biophys Acta (2000) 0.94
The effects of propofol on the contractility of failing and nonfailing human heart muscles. Anesth Analg (2001) 0.93
The myocardial protein S100A1 plays a role in the maintenance of normal gene expression in the adult heart. Mol Cell Biochem (2003) 0.90
Duration of left ventricular assist device support: Effects on abnormal calcium cycling and functional recovery in the failing human heart. J Heart Lung Transplant (2009) 0.90
S100A1 gene therapy for heart failure: a novel strategy on the verge of clinical trials. J Mol Cell Cardiol (2010) 0.87
Calcium cycling proteins and their association with heart failure. Clin Pharmacol Ther (2011) 0.86
Beta-adrenergic receptors and calcium cycling proteins in non-failing, hypertrophied and failing human hearts: transition from hypertrophy to failure. J Mol Cell Cardiol (2001) 0.83