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Special Issue "Updates on Erythropoietin"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: 29 February 2024 | Viewed by 806

Special Issue Editor

Division of Internal Medicine, Kitasato University Medical Center, 6-100 Arai, Kitamoto, Saitama 364-8501, Japan
Interests: erythropoietin; hypoxia; renal anemia; acid-base balance; hypertension

Special Issue Information

Dear Colleagues, 

Red blood cells carry oxygen to all organs in the body. Hypoxia and anemia cause cell damage and finally result in cell death. Erythropoietin (Epo) is produced via the activation of HIF2a and downregulation of PHD2 by hypoxia and anemia. Erythropoiesus-stimulating agent (ESA) and PHD inhibitors were used to substitute the erythrpoietic effects of Epo for patients with renal anemia. Epo has many effects on cellular function other than the production of blood cells. After many large-scale studies, ESAs were found not to have renoprotective effects. However, PHD inhibitors have renoprotective effects, especially in cases of ishchemic reperfusion injury. Although exogenous Epo (ESAs) does not have renoprotective effects, endogenous Epo produced by PHD inhibitors has renoprotective effects, suggesting that the HIF-PHD-Epo cascade is related to cell survival. The purpose of this Special Issue is to gather various data on the HIF-PHD-Epo cascade to discuss the role of endogenous Epo in cell survival against hypoxia.

Dr. Hiroshi Nonoguchi
Guest Editor

Manuscript Submission Information

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Keywords

  • erythropoietin (Epo)
  • hypoxia
  • hypoxia-inducible factor (HIF)
  • prolyl hydroxylase domain (PHD) inhibitor
  • chronic kidney disease (CKD)
  • anemia
  • erythropoiesus-stimulating agent (ESA)

Published Papers (1 paper)

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Research

Article
Changes in Metabolomic Profiles Induced by Switching from an Erythropoiesis-Stimulating Agent to a Hypoxia-Inducible Factor Prolyl Hydroxylase Inhibitor in Hemodialysis Patients: A Pilot Study
Int. J. Mol. Sci. 2023, 24(16), 12752; https://doi.org/10.3390/ijms241612752 - 13 Aug 2023
Viewed by 596
Abstract
Hypoxia-inducible factor prolyl hydroxylase inhibitors (HIF-PHIs) are a new class of medications for managing renal anemia in patients with chronic kidney disease (CKD). In addition to their erythropoietic activity, HIF-PHIs exhibit multifaceted effects on iron and glucose metabolism, mitochondrial metabolism, and angiogenesis through [...] Read more.
Hypoxia-inducible factor prolyl hydroxylase inhibitors (HIF-PHIs) are a new class of medications for managing renal anemia in patients with chronic kidney disease (CKD). In addition to their erythropoietic activity, HIF-PHIs exhibit multifaceted effects on iron and glucose metabolism, mitochondrial metabolism, and angiogenesis through the regulation of a wide range of HIF-responsive gene expressions. However, the systemic biological effects of HIF-PHIs in CKD patients have not been fully explored. In this prospective, single-center study, we comprehensively investigated changes in plasma metabolomic profiles following the switch from an erythropoiesis-stimulating agent (ESA) to an HIF-PHI, daprodustat, in 10 maintenance hemodialysis patients. Plasma metabolites were measured before and three months after the switch from an ESA to an HIF-PHI. Among 106 individual markers detected in plasma, significant changes were found in four compounds (erythrulose, n-butyrylglycine, threonine, and leucine), and notable but non-significant changes were found in another five compounds (inositol, phosphoric acid, lyxose, arabinose, and hydroxylamine). Pathway analysis indicated decreased levels of plasma metabolites, particularly those involved in phosphatidylinositol signaling, ascorbate and aldarate metabolism, and inositol phosphate metabolism. Our results provide detailed insights into the systemic biological effects of HIF-PHIs in hemodialysis patients and are expected to contribute to an evaluation of the potential side effects that may result from long-term use of this class of drugs. Full article
(This article belongs to the Special Issue Updates on Erythropoietin)
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