Late Na+ current and protracted electrical recovery are critical determinants of the aging myopathy

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Late Na+ current and protracted electrical recovery are critical determinants of the aging myopathy

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Title: Late Na+ current and protracted electrical recovery are critical determinants of the aging myopathy
Author: Signore, Sergio; Sorrentino, Andrea; Borghetti, Giulia; Cannata, Antonio; Meo, Marianna; Zhou, Yu; Kannappan, Ramaswamy; Pasqualini, Francesco; O'Malley, Heather; Sundman, Mark; Tsigkas, Nikolaos; Zhang, Eric; Arranto, Christian; Mangiaracina, Chiara; Isobe, Kazuya; Sena, Brena F.; Kim, Junghyun; Goichberg, Polina; Nahrendorf, Matthias; Isom, Lori L.; Leri, Annarosa; Anversa, Piero; Rota, Marcello

Note: Order does not necessarily reflect citation order of authors.

Citation: Signore, S., A. Sorrentino, G. Borghetti, A. Cannata, M. Meo, Y. Zhou, R. Kannappan, et al. 2015. “Late Na+ current and protracted electrical recovery are critical determinants of the aging myopathy.” Nature Communications 6 (1): 8803. doi:10.1038/ncomms9803. http://dx.doi.org/10.1038/ncomms9803.
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Abstract: The aging myopathy manifests itself with diastolic dysfunction and preserved ejection fraction. We raised the possibility that, in a mouse model of physiological aging, defects in electromechanical properties of cardiomyocytes are important determinants of the diastolic characteristics of the myocardium, independently from changes in structural composition of the muscle and collagen framework. Here we show that an increase in the late Na+ current (INaL) in aging cardiomyocytes prolongs the action potential (AP) and influences temporal kinetics of Ca2+ cycling and contractility. These alterations increase force development and passive tension. Inhibition of INaL shortens the AP and corrects dynamics of Ca2+ transient, cell contraction and relaxation. Similarly, repolarization and diastolic tension of the senescent myocardium are partly restored. Thus, INaL offers inotropic support, but negatively interferes with cellular and ventricular compliance, providing a new perspective of the biology of myocardial aging and the aetiology of the defective cardiac performance in the elderly.
Published Version: doi:10.1038/ncomms9803
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4638135/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:23993489
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