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.
journal_name
Sci Repjournal_title
Scientific reportsauthors
Liu J,Tian J,Chaudhry M,Maxwell K,Yan Y,Wang X,Shah PT,Khawaja AA,Martin R,Robinette TJ,El-Hamdani A,Dodrill MW,Sodhi K,Drummond CA,Haller ST,Kennedy DJ,Abraham NG,Xie Z,Shapiro JIdoi
10.1038/srep34592subject
Has Abstractpub_date
2016-10-04 00:00:00pages
34592issn
2045-2322pii
srep34592journal_volume
6pub_type
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