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Toxins
Special Issues
Uremic Metabolites
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Uremic Metabolites

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

Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 2462

Special Issue Editor

Dr. Terence Ryan

E-Mail Website
Guest Editor
Department of Applied Physiology & Kinesiology, University of Florida, Gainesville, FL 32611, USA
Interests: mitochondria; bioenergetics; redox biology; skeletal muscle; cardiovascular disease

Special Issue Information

Dear Colleagues,

A major function of the kidneys is to rid the body of waste materials that are either ingested or produced endogenously by normal metabolism. Impaired kidney function leads to the retention of waste products, termed uremic toxins, which can be harmful/toxic to numerous tissues/organs. Several uremic toxins have been strongly linked to cardiovascular and all-cause mortality in patients with renal insufficiency. Studies have also demonstrated pathological effects of these uremic toxins in numerous cell and tissue types. Despite what has been discovered, there is still very little known about the numerous mechanisms linking uremia to the pathogenesis of disease. Further to this, advancements in metabolomics technology have pushed the field to the precipice of identifying new uremic toxins with deleterious effects. This Special Issue will focus on publishing and highlighting original research articles and reviews on uremic toxicity, including their harmful effects in cells, tissue, animals, and patients, as well as cellular mechanisms of pathogenesis and novel therapeutics to ameliorate the effects of uremic toxins.

Sincerely,

Dr. Terence Ryan
Guest Editor

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

  • uremia
  • kidney disease
  • toxins
  • cardiovascular disease
  • metabolism
  • renal
  • dialysis
  • metabolomics
  • organic metabolites

Published Papers (1 paper)

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Research

16 pages, 4631 KiB  
Article
Pyroptosis: A Common Feature of Immune Cells of Haemodialysis Patients
by Christof Ulrich, Leonie Kneser, Roman Fiedler, Julia Beckert, Susann Wildgrube, Eric Seibert, Sylvia Fick, Christoph Schäfer, Silke Markau, Bogusz Trojanowicz and Matthias Girndt
Toxins 2021, 13(12), 839; https://0-doi-org.brum.beds.ac.uk/10.3390/toxins13120839 - 25 Nov 2021
Cited by 4 | Viewed by 2113
Abstract
NLRP-3 inflammasome activation can result in interleukin-1β (IL-1β) release and inflammatory cell death (pyroptosis). Caspase-1 is able to trigger both processes. However, other caspases, caspase-4, -5 and -8, are believed to initiate pyroptosis without affecting IL-1 secretion. In this study, we evaluated two [...] Read more.
NLRP-3 inflammasome activation can result in interleukin-1β (IL-1β) release and inflammatory cell death (pyroptosis). Caspase-1 is able to trigger both processes. However, other caspases, caspase-4, -5 and -8, are believed to initiate pyroptosis without affecting IL-1 secretion. In this study, we evaluated two cardiovascular risk groups, haemodialysis patients (HD) and patients with intact kidney function but high blood pressure (BP), to analyse the mechanisms driving pyroptosis. Twenty HD were age-, gender- and diabetes-matched to BP. We found a common pyroptotic pattern in both patient groups, at which pyroptosis rates but not IL-1 β levels were significantly higher in monocytes (HD vs. BP: p < 0.05), granulocytes (p < 0.01) and lymphocytes (p < 0.01) of HD patients. As uremic toxins are drivers of inflammation and regulated cell death, we applied a monocyte- and macrophage-like THP-1 model system to demonstrate that the protein-bound uremic toxin indoxyl sulfate (IS) is an inducer of pyroptotic cell death, particularly engaging caspase-4/caspase-5 and to a lesser extent caspase-8 and caspase-1. These data suggest that the uremic toxin IS can mediate pyroptosis in HD patients and the inflammatory caspase-4 and/or caspase-5 contribute to pyroptosis rates to a higher extent in comparison to caspase-1. Full article
(This article belongs to the Special Issue Uremic Metabolites)
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