Why the study?
Does parvalbumin gene delivery improve myocardial relaxation performance in adult rats?
Does parvalbumin gene delivery improve myocardial relaxation performance in adult rats?
In vivo parvalbumin gene transfer accelerates myocardial relaxation in normal hearts and restores relaxation performance in a model of slowed cardiac relaxation, offering a potential ATP-independent therapeutic approach for diastolic dysfunction in heart failure.
Hypothesis-generating for parvalbumin-based therapy in diastolic dysfunction; requires validation before any clinical consideration.
Defective cardiac muscle relaxation plays a causal role in heart failure. Shown here is the new in vivo application of parvalbumin, a calcium-binding protein that facilitates ultrafast relaxation of specialized skeletal muscles. Parvalbumin is not naturally expressed in the heart. We show that parvalbumin gene transfer to the heart in vivo produces levels of parvalbumin characteristic of fast skeletal muscles, causes a physiologically relevant acceleration of heart relaxation performance in normal hearts, and enhances relaxation performance in an animal model of slowed cardiac muscle relaxation. Parvalbumin may offer the unique potential to correct defective relaxation in energetically compromised failing hearts because the relaxation-enhancement effect of parvalbumin arises from an ATP-independent mechanism. Additionally, parvalbumin gene transfer may provide a new therapeutic approach to correct cellular disturbances in calcium signaling pathways that cause abnormal growth or damage in the heart or other organs.
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Szatkowski et al. (2001) studied this question.
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