Corrigendum: Attenuation of Na/K-ATPase Mediated Oxidant Amplification with pNaKtide Ameliorates Experimental Uremic Cardiomyopathy

نویسندگان

  • Jiang Liu
  • Jiang Tian
  • Muhammad Chaudhry
  • Kyle Maxwell
  • Yanling Yan
  • Xiaoliang Wang
  • Preeya T. Shah
  • Asad A. Khawaja
  • Rebecca Martin
  • Tylor J. Robinette
  • Adee El-Hamdani
  • Michael W. Dodrill
  • Komal Sodhi
  • Christopher A. Drummond
  • Steven T. Haller
  • David J. Kennedy
  • Nader G. Abraham
  • Zijian Xie
  • Joseph I. Shapiro
چکیده

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.

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عنوان ژورنال:

دوره 7  شماره 

صفحات  -

تاریخ انتشار 2016