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The idiopathic dilated cardiomyopathy in man. A biochemical and molecular study on myosin
L Dalla Libera1, P Pauletto, D Piccolo
1C.N.R. Centro di Studio per la Biologia e Fisiopatologia Muscolare, Università di Padova, Italia.
Insights
This study investigated myosin in hearts with dilated cardiomyopathy, finding atrial-like light chain 1 (ALC1) was absent in ventricles. However, ventricular-like light chain 2 (VLC2) was present in atria, correlating with depressed ATPase activity.
Area of Science:
- Cardiology
- Molecular Biology
- Biochemistry
Background:
- Idiopathic dilated cardiomyopathy (IDC) affects heart muscle function.
- Myosin's role in cardiac contraction is critical, with varying subunit compositions potentially influencing contractile properties.
Purpose of the Study:
- To investigate the myosin subunit composition and Ca(++)-activated ATPase activity in atrial and ventricular tissues from hearts with IDC.
- To determine if the absence of myosin atrial-like light chain 1 (ALC1) in ventricular tissue and the presence of ventricular-like light chain 2 (VLC2) in atrial tissue are associated with altered cardiac function in IDC.
Main Methods:
- Myosin isolation from explanted human hearts (atria and ventricles) of patients with IDC.
- Analysis of myosin subunit composition using two-dimensional electrophoresis and immunoblotting.
- Measurement of Ca(++)-activated ATPase activity of isolated myosin.
Main Results:
- Myosin atrial-like light chain 1 (ALC1) was not detected in ventricular subendocardial, septal, or subepicardial layers of IDC hearts.
- Ventricular-like light chain 2 (VLC2) was identified in both atrial and ventricular myosin from IDC hearts.
- A depressed Ca(++)-activated ATPase activity was observed in both atrial and ventricular myosin from IDC patients compared to controls.
Conclusions:
- The absence of ALC1 in ventricular myosin and the presence of VLC2 in atrial myosin in IDC hearts may contribute to altered cardiac mechanics.
- Depressed Ca(++)-activated ATPase activity in atrial myosin from IDC hearts is linked to the expression of ventricular-type myosin heavy chains and VLC2.
- The cause of depressed ATPase activity in ventricular myosin in IDC remains unclear, as myosin heavy and light chains showed no significant differences compared to controls.
Abstract:
We studied subunit composition and Ca(++)-activated ATPase activity of myosin isolated from atria and ventricles of hearts explanted from patients suffering from idiopathic dilated cardiomyopathy. At variance with previously published data, we have been unable to detect in the ventricular subendocardial layers a significant amount of myosin atrial-like light chain 1 (ALC1), which has been reported to be related to some hemodynamic features of the hypertrophied and failing heart. Such a subunit was not visible in the septum and in the subepicardial layers either. On the contrary, in both atria a ventricular-like light chain 2 (VLC2) was found. The nature of this additional light chain was confirmed on the basis of two-dimensional electrophoresis and immunoblotting techniques with polyclonal antibodies reacting with VLC2. In these patients we also observed a depressed Ca(++)-activated ATPase activity, both in atrial and ventricular myosin. The explanation for this finding in ventricles still remains obscure since neither myosin light chains, nor myosin heavy chains showed any difference between patients with dilated cardiomyopathy and controls. On the contrary, in atria we clearly identified changes consistent with the expression of myosin heavy chains of ventricular type and VLC2, which can account for the depressed Ca(++)-activated ATPase activity.
Related Concept Videos
Overview of Myosin Structure and Function
Myocarditis I: Introduction
Cardiomyopathy II: Dilated Cardiomyopathy
Cardiomyopathy III: Hypertrophic Cardiomyopathy
Cardiomyopathy IV: Restrictive Cardiomyopathy
Cardiomyopathy V: Interprofessional Care

