NYMC Faculty Publications
First Page
34592
Last Page
34592
Document Type
Article
Publication Date
10-4-2016
Department
Medicine
Abstract
We have previously reported that the sodium potassium adenosine triphosphatase (Na/K-ATPase) can effect the amplification of reactive oxygen species. In this study, we examined whether attenuation of oxidant stress by antagonism of Na/K-ATPase oxidant amplification might ameliorate experimental uremic cardiomyopathy induced by partial nephrectomy (PNx). PNx induced the development of cardiac morphological and biochemical changes consistent with human uremic cardiomyopathy. Both inhibition of Na/K-ATPase oxidant amplification with pNaKtide and induction of heme oxygenase-1 (HO-1) with cobalt protoporphyrin (CoPP) markedly attenuated the development of phenotypical features of uremic cardiomyopathy. In a reversal study, administration of pNaKtide after the induction of uremic cardiomyopathy reversed many of the phenotypical features. Attenuation of Na/K-ATPase oxidant amplification may be a potential strategy for clinical therapy of this disorder.
Recommended Citation
Liu, J., Tian, J., Chaudhry, M., Maxwell, K., Yan, Y., Wang, X., . . . Shapiro, J. I. (2016). Attenuation of Na/K-ATPase mediated oxidant amplification with pNaKtide ameliorates experimental uremic cardiomyopathy. Scientific Reports, 6, Art. No.: 34592. doi:10.1038/srep34592
Publisher's Statement
Originally published in Scientific Reports. Licensed under CC-BY 4.0. https://doi.org/10.1038/srep34592
Comments
Please see the work itself for the complete list of authors.