Diltiazem prevents stress‐induced contractile deficits in cardiomyocytes, but does not reverse the cardiomyopathy phenotype in Mybpc3‐knock‐in mice

Key points Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac illness and can lead to diastolic dysfunction, sudden cardiac death and heart failure. Treatment of HCM patients is empirical and current pharmacological treatments are unable to stop disease progression or reverse hyp...

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Veröffentlicht in:	The Journal of physiology 2017-06, Vol.595 (12), p.3987-3999
Hauptverfasser:	Flenner, Frederik, Geertz, Birgit, Reischmann‐Düsener, Silke, Weinberger, Florian, Eschenhagen, Thomas, Carrier, Lucie, Friedrich, Felix W.
Format:	Artikel
Sprache:	eng
Schlagworte:	Activation Adrenergic receptors Animals Antagonists Arrhythmia Calcium - metabolism Calcium antagonists cardiac myosin‐binding protein C Cardiomyocytes Cardiomyopathy Cardiomyopathy, Hypertrophic - metabolism Carrier Proteins - metabolism Contractility Contraction Death Diastole - drug effects Dihydropyridine Diltiazem Diltiazem - pharmacology Drug therapy Effectiveness Eutrophication Fetuses Fibrosis Genotype & phenotype Guidelines Heart Heart diseases Heart failure Heart Ventricles - drug effects Heart Ventricles - metabolism hypertrophic cardiomyopathy Hypertrophy Isoproterenol - pharmacology Knock Mice Muscle contraction Mutation Mutation - genetics Myocardial Contraction - drug effects Myocardium - metabolism Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Phenotype Pretreatment Regulation of Contractile Function in Health and Disease Rodents Sarcomeres - drug effects Sarcomeres - metabolism Stress relaxation Symposium Related Research Paper Ventricle
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