Special Issue "Role of Uremic Toxins in Vascular Calcification, Vascular Disease and Bone Dysfunction"
Deadline for manuscript submissions: 31 October 2020.
Interests: Uremic toxins; pharmaco-epidemiology, cardiovascular; vascular calcification
Interests: uremic toxins; cardiovascular; bone; vascular calcification; endothelium
Special Issues and Collections in MDPI journals
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
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.
- uremic toxins
- vascular calcification
- vascular stiffness
- bone dysfunction
- chronic kidney disease
- bone mineral disorder
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.