Special Issue "Role of Uremic Toxins in Vascular Calcification, Vascular Disease and Bone Dysfunction"

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

Deadline for manuscript submissions: 31 October 2020.

Special Issue Editors

Prof. Sophie Liabeuf
Website
Guest Editor
Division of Clinical Pharmacology, Amiens University Medical Center, Amiens, France and EA7517 Unit— MP3CV, UPJV University, Amiens, France
Interests: Uremic toxins; pharmaco-epidemiology, cardiovascular; vascular calcification
Prof. Ziad A. Massy
Website
Guest Editor
Division of Nephrology, Ambroise Paré Hospital, APHP, Paris-Ile-de-France-West Versailles-Saint-Quentin-en-Yvelines University (UVSQ), 9 avenue Charles de Gaulle, 92104 Boulogne Billancourt/Paris and Inserm U1018 Team5, CESP, UVSQ, University Paris Saclay, Villejuif, France
Interests: uremic toxins; cardiovascular; bone; vascular calcification; endothelium
Special Issues and Collections in MDPI journals

Special Issue Information

Dear Colleagues,

Chronic kidney disease (CKD) is a global public health problem that is associated with major adverse health events, including kidney failure, cardiovascular disease and death. Due to the low life expectancy and high prevalence of comorbidities in patients with CKD, research in this field is focusing on the identification of modifiable risk factors. Uremic retention solutes may constitute important non-traditional risk factors in this population. The members of this large group of solutes (referred to as “uremic toxins” when they perturb normal biological functions) differ in their water solubility, protein-binding capacity, molecular weight, pattern of removal by dialysis, biological properties and ability to produce clinical symptoms. Three subgroups of uremic toxins have been suggested: small molecules (e.g., urea and phosphate), mid-sized molecules (e.g., fibroblast growth factor 23 (FGF23)) and protein-bound uremic toxins (e.g., p-cresylsulfate (PCS) and indoxylsulfate (IS)).

CKD is associated with extensive vascular calcification, vascular disease and abnormal bone remodelling. Moreover, growing evidence points towards a close relationship between bone and vessel. Some evidence has suggested that uremic toxins could impact the kidney–cardiovascular–bone axis.

The focus of this Special Issue of Toxins will include original research articles and reviews on the role of Uremic Toxins in Vascular Calcification, Vascular disease and Bone Dysfunction in these different aspects.

Prof. Sophie Liabeuf
Prof. Ziad Massy
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 papers will be 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 2000 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
  • vascular calcification
  • vascular stiffness
  • endothelium
  • bone dysfunction
  • chronic kidney disease
  • bone mineral disorder

Published Papers (2 papers)

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Review

Open AccessReview
How do Uremic Toxins Affect the Endothelium?
Toxins 2020, 12(6), 412; https://doi.org/10.3390/toxins12060412 - 20 Jun 2020
Abstract
Uremic toxins can induce endothelial dysfunction in patients with chronic kidney disease (CKD). Indeed, the structure of the endothelial monolayer is damaged in CKD, and studies have shown that the uremic toxins contribute to the loss of cell–cell junctions, increasing permeability. Membrane proteins, [...] Read more.
Uremic toxins can induce endothelial dysfunction in patients with chronic kidney disease (CKD). Indeed, the structure of the endothelial monolayer is damaged in CKD, and studies have shown that the uremic toxins contribute to the loss of cell–cell junctions, increasing permeability. Membrane proteins, such as transporters and receptors, can mediate the interaction between uremic toxins and endothelial cells. In these cells, uremic toxins induce oxidative stress and activation of signaling pathways, including the aryl hydrocarbon receptor (AhR), nuclear factor kappa B (NF-κB), and mitogen-activated protein kinase (MAPK) pathways. The activation of these pathways leads to overexpression of proinflammatory (e.g., monocyte chemoattractant protein-1, E-selectin) and prothrombotic (e.g., tissue factor) proteins. Uremic toxins also induce the formation of endothelial microparticles (EMPs), which can lead to the activation and dysfunction of other cells, and modulate the expression of microRNAs that have an important role in the regulation of cellular processes. The resulting endothelial dysfunction contributes to the pathogenesis of cardiovascular diseases, such as atherosclerosis and thrombotic events. Therefore, uremic toxins as well as the pathways they modulated may be potential targets for therapies in order to improve treatment for patients with CKD. Full article
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Open AccessReview
Uremic Toxins and Vascular Dysfunction
Toxins 2020, 12(6), 404; https://doi.org/10.3390/toxins12060404 - 18 Jun 2020
Abstract
Vascular dysfunction is an essential element found in many cardiovascular pathologies and in pathologies that have a cardiovascular impact such as chronic kidney disease (CKD). Alteration of vasomotricity is due to an imbalance between the production of relaxing and contracting factors. In addition [...] Read more.
Vascular dysfunction is an essential element found in many cardiovascular pathologies and in pathologies that have a cardiovascular impact such as chronic kidney disease (CKD). Alteration of vasomotricity is due to an imbalance between the production of relaxing and contracting factors. In addition to becoming a determining factor in pathophysiological alterations, vascular dysfunction constitutes the first step in the development of atherosclerosis plaques or vascular calcifications. In patients with CKD, alteration of vasomotricity tends to emerge as being a new, less conventional, risk factor. CKD is characterized by the accumulation of uremic toxins (UTs) such as phosphate, para-cresyl sulfate, indoxyl sulfate, and FGF23 and, consequently, the deleterious role of UTs on vascular dysfunction has been explored. This accumulation of UTs is associated with systemic alterations including inflammation, oxidative stress, and the decrease of nitric oxide production. The present review proposes to summarize our current knowledge of the mechanisms by which UTs induce vascular dysfunction. Full article
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: Molecular Mechanism of Indoxyl Sulfate-Induced Adipose Tissue Inflammation
Authors: Hiroshi Watanabe
Affiliation: Kumamoto University, Japan

Title: Uremic Toxins and Vascular Dysfunction
Authors: Isabelle Six
Affiliation: Jules Verne University of Picardie, Amiens, France
Abstract: The vascular dysfunction is an essential element found in many cardiovascular pathologies and those having a cardiovascular impact such as chronic kidney disease (CKD). The vascular dysfunction is due to the break in balance between vasorelaxing and vasoconstrictor factors produced. In addition to be a determining factor in pathophysiological alterations, vascular dysfunction would constitute the first step for the development of atherosclerosis plaques or vascular calcifications. In patients with CKD, vascular dysfunction tends to emerge as being a new, less conventional, risk factor. In CKD, this dysfunction is associated with systemic alterations including an inflammation, an oxidative stress, a reactive oxygen species modulation, a decrease in nitric oxide (NO) production as well as an increased production of asymmetric dimethylarginine, an endogenous inhibitor of NO synthase. CKD is also characterized by the accumulation of Protein-bound uremic toxins (UTs) like phosphate, indoxyl sulfate or paracresyl sulfate and consequently the deleterious role of UTs on vascular dysfunction has been explored. This review proposes to summarize our current knowledge on the mechanisms by which UTs induced vascular dysfunction

Title: Role of Uremic Toxins in Vascular Calcification and Early Vascular Ageing
Authors: Nikolaos C. Kyriakidis 1, Gabriela Cobo 2, Lu Dai 3, Bengt Lindholm 3, Peter Stenvinkel 3
Affiliation: 1. Facultad de Ciencias de la Salud, Escuela de Medicina, Grupo de Investigación en Biotecnología Aplicada a Biomedicina (BIOMED), Universidad de Las Américas (UDLA), Quito, Ecuador;

2. Nephrology Department, Hospital de Especialidades Eugenio Espejo, Quito, Ecuador;

3. Division of Renal Medicine and Baxter Novum, Department of Clinical Science, Intervention and Technology, Karolinska Institutet, Campus Flemingsberg, Stockholm, Sweden;


Abstract: The accumulation of uremic toxins, caused by a combination of decreased excretion secondary to reduced kidney function as well as aberrant expression of metabolite genes, interfere with different biological functions and have been associated with chronic inflammation and tissue damage. Uremic toxins have been implicated in severe vascular smooth muscle cells (VSMCs) changes leading to media vascular calcification. Vascular calcification and early vascular ageing are predominant clinical features of chronic kidney disease (CKD) patients, resulting in an exceptionally high premature cardiovascular mortality. We discuss the latest updates on the pathophysiological processes underlying vascular calcification and early vascular ageing induced by uremic toxins, clinical impact and possible therapeutic targets.

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