Cellular basis of abnormal calcium transients of failing human ventricular myocytes.
about
ESC working group cellular biology of the heart: position paper: improving the preclinical assessment of novel cardioprotective therapiesEnhancing calstabin binding to ryanodine receptors improves cardiac and skeletal muscle function in heart failure.The human subject: an integrative animal model for 21(st) century heart failure researchModeling cardiac electromechanics and mechanoelectrical coupling in dyssynchronous and failing hearts: insight from adaptive computer modelsIon Channels in the HeartAbnormal Ca(2+) cycling in failing ventricular myocytes: role of NOS1-mediated nitroso-redox balanceCalmodulin-dependent protein kinase II: linking heart failure and arrhythmiasMechanisms of altered Ca²⁺ handling in heart failureExamination of the Effects of Heterogeneous Organization of RyR Clusters, Myofibrils and Mitochondria on Ca2+ Release Patterns in CardiomyocytesThe second Ca2+-binding domain of the Na+ Ca2+ exchanger is essential for regulation: crystal structures and mutational analysis."Freeze, Don't Move": How to Arrest a Suspect in Heart Failure - A Review on Available GRK2 InhibitorsConnective tissue growth factor overexpression in cardiomyocytes promotes cardiac hypertrophy and protection against pressure overloadGender differences in the modulation of cardiac gene expression by dietary conjugated linoleic acid isomersA peptide encoded by a transcript annotated as long noncoding RNA enhances SERCA activity in muscleSmall and large animal models in cardiac contraction research: advantages and disadvantagesSimulation and mechanistic investigation of the arrhythmogenic role of the late sodium current in human heart failureEndothelial dysfunction is associated with left ventricular mass (assessed using MRI) in an adult population (MESA).G protein-coupled receptor kinase 2 ablation in cardiac myocytes before or after myocardial infarction prevents heart failure.Survival and maturation of human embryonic stem cell-derived cardiomyocytes in rat heartsRecapitulating maladaptive, multiscale remodeling of failing myocardium on a chip.Differential effects of S100 proteins A2 and A6 on cardiac Ca(2+) cycling and contractile performance.Thin filament incorporation of an engineered cardiac troponin C variant (L48Q) enhances contractility in intact cardiomyocytes from healthy and infarcted hearts.Microdomain-Specific Modulation of L-Type Calcium Channels Leads to Triggered Ventricular Arrhythmia in Heart Failure.Dilated cardiomyopathy with increased SR Ca2+ loading preceded by a hypercontractile state and diastolic failure in the alpha(1C)TG mouse.Local control of excitation-contraction coupling in human embryonic stem cell-derived cardiomyocytes.Role of RyR2 phosphorylation in heart failure and arrhythmias: protein kinase A-mediated hyperphosphorylation of the ryanodine receptor at serine 2808 does not alter cardiac contractility or cause heart failure and arrhythmiasInfluence of a constitutive increase in myofilament Ca(2+)-sensitivity on Ca(2+)-fluxes and contraction of mouse heart ventricular myocytesCaV1.2 beta-subunit coordinates CaMKII-triggered cardiomyocyte death and afterdepolarizationsThere goes the neighborhood: pathological alterations in T-tubule morphology and consequences for cardiomyocyte Ca2+ handling.Impact of sarcoplasmic reticulum calcium release on calcium dynamics and action potential morphology in human atrial myocytes: a computational study.Exercise training corrects control of spontaneous calcium waves in hearts from myocardial infarction heart failure rats.Circulating miR-323-3p is a biomarker for cardiomyopathy and an indicator of phenotypic variability in Friedreich's ataxia patients.Early remodeling of perinuclear Ca2+ stores and nucleoplasmic Ca2+ signaling during the development of hypertrophy and heart failure.Late sodium current contributes to diastolic cell Ca2+ accumulation in chronic heart failure.Systems approach to understanding electromechanical activity in the human heart: a national heart, lung, and blood institute workshop summary.Rate-dependent action potential alternans in human heart failure implicates abnormal intracellular calcium handling.Inhibition of miR-25 improves cardiac contractility in the failing heart.Overexpression of junctophilin-2 does not enhance baseline function but attenuates heart failure development after cardiac stress.Enhanced basal contractility but reduced excitation-contraction coupling efficiency and beta-adrenergic reserve of hearts with increased Cav1.2 activity.A computational model of the human left-ventricular epicardial myocyte.
P2860
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P2860
Cellular basis of abnormal calcium transients of failing human ventricular myocytes.
description
2003 nî lūn-bûn
@nan
2003年の論文
@ja
2003年学术文章
@wuu
2003年学术文章
@zh
2003年学术文章
@zh-cn
2003年学术文章
@zh-hans
2003年学术文章
@zh-my
2003年学术文章
@zh-sg
2003年學術文章
@yue
2003年學術文章
@zh-hant
name
Cellular basis of abnormal calcium transients of failing human ventricular myocytes.
@en
Cellular basis of abnormal calcium transients of failing human ventricular myocytes.
@nl
type
label
Cellular basis of abnormal calcium transients of failing human ventricular myocytes.
@en
Cellular basis of abnormal calcium transients of failing human ventricular myocytes.
@nl
prefLabel
Cellular basis of abnormal calcium transients of failing human ventricular myocytes.
@en
Cellular basis of abnormal calcium transients of failing human ventricular myocytes.
@nl
P2093
P50
P1433
P1476
Cellular basis of abnormal calcium transients of failing human ventricular myocytes.
@en
P2093
Jutta Weisser-Thomas
Kenneth B Margulies
Steven R Houser
Valentino Piacentino
P304
P356
10.1161/01.RES.0000062469.83985.9B
P577
2003-02-20T00:00:00Z