Blockage of the Na-K-ATPase signaling-mediated oxidant amplification loop elongates red blood cell half-life and ameliorates uremic anemia induced by 5/6th PNx in C57BL/6 mice

Author:

Liu Jiang1ORCID,Chaudhry Muhammad1ORCID,Bai Fang1,Chuang Justin2,Chaudhry Hibba1,Al-Astal Ala-Eddin Yassin1ORCID,Nie Ying1,Sollars Vincent1,Sodhi Komal3,Seligman Paul4,Shapiro Joseph I.2

Affiliation:

1. Department of Biomedical Sciences, Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia

2. Department of Medicine, Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia

3. Department of Surgery, Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia

4. Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado

Abstract

The anemia of CKD is multifactorial, and the current treatment based primarily on stimulating bone marrow production of RBCs with erythropoietin of erythropoietin analogs is unsatisfactory. In a murine model of CKD that is complicated by anemia, blockade of Na-K-ATPase signaling with a specific peptide (pNaKtide) ameliorated the anemia primarily by increasing RBC survival. Should these results be confirmed in patients, this strategy may allow for novel and potentially additive strategies to treat the anemia of CKD.

Funder

HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases

HHS | NIH | National Heart, Lung, and Blood Institute

HHS | NIH | National Institute of General Medical Sciences

Huntington Foundation

BrickStreet Foundation

Publisher

American Physiological Society

Subject

Physiology

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