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Toxins
Special Issues
The Functional Analysis of Uremic Toxins by Metabolomics 2.0
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The Functional Analysis of Uremic Toxins by Metabolomics 2.0

A special issue of Toxins (ISSN 2072-6651). This special issue belongs to the section "Uremic Toxins".

Deadline for manuscript submissions: closed (30 October 2022) | Viewed by 4396

Special Issue Editors

Dr. Emiko Sato

E-Mail Website
Guest Editor
Tohoku University | Division of Clinical Pharmacology and Therapeutics, Graduate School of Pharmaceutical Sciences, Sendai, Japan
Interests: uremic toxins; metabolomic analysis; uremic toxins-related organ damage; indoxyl sulphate
Special Issues, Collections and Topics in MDPI journals
Dr. Daisuke Saigusa

E-Mail Website
Guest Editor
Laboratory of Biomedical and Analytical Sciences, Faculty of Pharma-Science, Teikyo University, Tokyo, Japan
Interests: liquid chromatography mass spectrometry; mass spectrometry imaging; metabolomics; lipidomics; microbiome; biomarker searching for kidney diseases

Special Issue Information

Dear Colleagues,

This is the second part of the Special Issue on “The Functional Analysis of Uremic Toxins by Metabolomics”.

A metabolomic analysis is the comprehensive analysis of small molecules within the body, known as metabolites, reflecting the underlying biochemical activity and state of cells or tissues. Thus, a metabolomic analysis using mass spectrometry is a powerful tool for capturing disease–metabolic signatures, widely used for biomarker discovery and the understanding of pathogenesis.

In the first part of the Special Issue (https://www.mdpi.com/journal/toxins/special_issues/uremic_metabolomics), we presented following studies using comprehensive mass spectrometry metabolomics.

Kumakura et al. reported on metabolic changes and uremic toxin levels in the body and kidneys during renal failure, and the improvement of these changes with the administration of therapeutic candidates using liquid chromatography or gas chromatography mass spectrometry-targeting metabolomics.

Akiyama et al. reported the profile of uremic solutes in hemodialysis patients using comprehensive capillary electrophoresis mass spectrometry metabolomics.

Hishinuma et al. reported the characteristic metabolic profiles of epithelial ovarian cancer (EOC) patients using comprehensive UHPLC-MS/MS metabolomics, and revealed that kynurenine, a uremic toxin, is associated with prognosis in EOC patients.

The Special Issue entitled “The Functional Analysis of Uremic Toxins by Metabolomics 2.0 ” also focuses on understanding the roles of uremic toxins regarding organ dysfunction in renal failure conditions, especially welcoming studies examining metabolic alterations by uremic toxins using cell lines, animal renal failure models, and clinical studies assessed by mass spectrometry, as well as studies visualizing the metabolic alteration and accumulated uremic toxins in tissues using imaging mass spectrometry.

Dr. Emiko Sato
Dr. Daisuke Saigusa
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a double-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Toxins is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • uremic toxins
  • metabolomics
  • indoxyl sulphate
  • p-cresyl sulfate
  • phenyl sulfate
  • uremic sarcopenia
  • cognitive impairment
  • mass spectrometry
  • chronic kidney disease
  • microbiome

Published Papers (1 paper)

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Research

14 pages, 1552 KiB  
Article
Methylglyoxal Induces Inflammation, Metabolic Modulation and Oxidative Stress in Myoblast Cells
by Sota Todoriki, Yui Hosoda, Tae Yamamoto, Mayu Watanabe, Akiyo Sekimoto, Hiroshi Sato, Takefumi Mori, Mariko Miyazaki, Nobuyuki Takahashi and Emiko Sato
Toxins 2022, 14(4), 263; https://doi.org/10.3390/toxins14040263 - 07 Apr 2022
Cited by 5 | Viewed by 4039
Abstract
Uremic sarcopenia is a serious clinical problem associated with physical disability and increased morbidity and mortality. Methylglyoxal (MG) is a highly reactive, dicarbonyl uremic toxin that accumulates in the circulatory system in patients with chronic kidney disease (CKD) and is related to the [...] Read more.
Uremic sarcopenia is a serious clinical problem associated with physical disability and increased morbidity and mortality. Methylglyoxal (MG) is a highly reactive, dicarbonyl uremic toxin that accumulates in the circulatory system in patients with chronic kidney disease (CKD) and is related to the pathology of uremic sarcopenia. The pathophysiology of uremic sarcopenia is multifactorial; however, the details remain unknown. We investigated the mechanisms of MG-induced muscle atrophy using mouse myoblast C2C12 cells, focusing on intracellular metabolism and mitochondrial injury. We found that one of the causative pathological mechanisms of uremic sarcopenia is metabolic flow change to fatty acid synthesis with MG-induced ATP shortage in myoblasts. Evaluation of cell viability revealed that MG showed toxic effects only in myoblast cells, but not in myotube cells. Expression of mRNA or protein analysis revealed that MG induces muscle atrophy, inflammation, fibrosis, and oxidative stress in myoblast cells. Target metabolomics revealed that MG induces metabolic alterations, such as a reduction in tricarboxylic acid cycle metabolites. In addition, MG induces mitochondrial morphological abnormalities in myoblasts. These changes resulted in the reduction of ATP derived from the mitochondria of myoblast cells. Our results indicate that MG is a pathogenic factor in sarcopenia in CKD. Full article
(This article belongs to the Special Issue The Functional Analysis of Uremic Toxins by Metabolomics 2.0)
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