In vivo acceleration of heart relaxation performance by parvalbumin gene delivery.
Publication/Presentation Date
1-1-2001
Abstract
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.
Volume
107
Issue
2
First Page
191
Last Page
198
ISSN
0021-9738
Published In/Presented At
Szatkowski, M. L., Westfall, M. V., Gomez, C. A., Wahr, P. A., Michele, D. E., DelloRusso, C., Turner, I. I., Hong, K. E., Albayya, F. P., & Metzger, J. M. (2001). In vivo acceleration of heart relaxation performance by parvalbumin gene delivery. The Journal of clinical investigation, 107(2), 191–198. https://doi.org/10.1172/JCI9862
Disciplines
Medicine and Health Sciences | Pediatrics
PubMedID
11160135
Department(s)
Department of Pediatrics
Document Type
Article