Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
4.0
4.2
Journals
Biology
Special Issues
Recent Advances in Vascular Calcification
share announcement

Recent Advances in Vascular Calcification

A special issue of Biology (ISSN 2079-7737).

Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 3565

Special Issue Editor

Dr. Ricardo Villa-Bellosta

E-Mail Website
Guest Editor
1. Center for Research in Molecular Medicine and Chronic Diseases (CiMUS), Av Barcelona. Campus Vida, Universidade de Santiago de Compostela, 15782 Santiago de Compostela, Spain
2. Department of Biochemistry and Molecular Biology, Universidade de Santiago de Compostela, Plaza do Obradoiro s/n, 15782 Santiago de Compostela, Spain
Interests: vascular calcification; aging; progeria; phosphate homeostasis; pyrophosphate homeostasis; ATP; diabetes; chronic kidney disease; Hutchinson-Gilford progeria syndrome; membrane transport

Special Issue Information

Dear Colleagues,

Cardiovascular diseases are the leading cause of global mortality and a major contributor to disability. Among them, calcification of the aortic wall is characterized by a pathological accumulation of phosphate–calcium crystals and by genetic and morphological changes in the vascular wall that could progress to aortic wall rupture, cardiovascular events, and deaths. Vascular calcification is strongly associated with aging, accelerated aging (progeria), chronic kidney disease, diabetes, and several rare diseases. The treatment of vascular calcification is mainly based on the control of different vascular calcification risk factors, but there is still an unmet need to find novel potential therapeutic targets to prevent the devastating effects of vascular calcification.

This Special Issue will summarize contributions that advance our understanding of the etiology of vascular calcification. We aim to highlight the involvement of genetic and functional changes in phosphate-induced smooth muscle calcification. We aim to also highlight the involvement of resident and infiltrated cells in the pathophysiology of both atheroma plaque and medial calcifications, including articles/reviews focused on specific cell types. In addition, we welcome contributions that advance our understanding of the molecular mechanisms of vascular calcification and potential new therapeutic approaches, with a particular emphasis on studies with potential human translation.

I look forward to receiving your contributions.

Dr. Ricardo Villa-Bellosta
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 single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biology 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

  • vascular calcification
  • aging
  • medial calcification
  • atheroma plaque calcification
  • chronic kidney disease
  • diabetes
  • phosphate

Published Papers (2 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Review

15 pages, 2672 KiB  
Review
Vascular Calcification: A Passive Process That Requires Active Inhibition
by Ricardo Villa-Bellosta
Biology 2024, 13(2), 111; https://doi.org/10.3390/biology13020111 - 9 Feb 2024
Cited by 2 | Viewed by 1706
Abstract
The primary cause of worldwide mortality and morbidity stems from complications in the cardiovascular system resulting from accelerated atherosclerosis and arterial stiffening. Frequently, both pathologies are associated with the pathological calcification of cardiovascular structures, present in areas such as cardiac valves or blood [...] Read more.
The primary cause of worldwide mortality and morbidity stems from complications in the cardiovascular system resulting from accelerated atherosclerosis and arterial stiffening. Frequently, both pathologies are associated with the pathological calcification of cardiovascular structures, present in areas such as cardiac valves or blood vessels (vascular calcification). The accumulation of hydroxyapatite, the predominant form of calcium phosphate crystals, is a distinctive feature of vascular calcification. This phenomenon is commonly observed as a result of aging and is also linked to various diseases such as diabetes, chronic kidney disease, and several genetic disorders. A substantial body of evidence indicates that vascular calcification involves two primary processes: a passive process and an active process. The physicochemical process of hydroxyapatite formation and deposition (a passive process) is influenced significantly by hyperphosphatemia. However, the active synthesis of calcification inhibitors, including proteins and low-molecular-weight inhibitors such as pyrophosphate, is crucial. Excessive calcification occurs when there is a loss of function in enzymes and transporters responsible for extracellular pyrophosphate metabolism. Current in vivo treatments to prevent calcification involve addressing hyperphosphatemia with phosphate binders and implementing strategies to enhance the availability of pyrophosphate. Full article
(This article belongs to the Special Issue Recent Advances in Vascular Calcification)
►▼ Show Figures

Figure 1

33 pages, 2639 KiB  
Review
The Purinergic Nature of Pseudoxanthoma Elasticum
by Gilles Kauffenstein, Ludovic Martin and Olivier Le Saux
Biology 2024, 13(2), 74; https://doi.org/10.3390/biology13020074 - 26 Jan 2024
Cited by 1 | Viewed by 1477
Abstract
Pseudoxanthoma Elasticum (PXE) is an inherited disease characterized by elastic fiber calcification in the eyes, the skin and the cardiovascular system. PXE results from mutations in ABCC6 that encodes an ABC transporter primarily expressed in the liver and kidneys. It took nearly 15 [...] Read more.
Pseudoxanthoma Elasticum (PXE) is an inherited disease characterized by elastic fiber calcification in the eyes, the skin and the cardiovascular system. PXE results from mutations in ABCC6 that encodes an ABC transporter primarily expressed in the liver and kidneys. It took nearly 15 years after identifying the gene to better understand the etiology of PXE. ABCC6 function facilitates the efflux of ATP, which is sequentially hydrolyzed by the ectonucleotidases ENPP1 and CD73 into pyrophosphate (PPi) and adenosine, both inhibitors of calcification. PXE, together with General Arterial Calcification of Infancy (GACI caused by ENPP1 mutations) as well as Calcification of Joints and Arteries (CALJA caused by NT5E/CD73 mutations), forms a disease continuum with overlapping phenotypes and shares steps of the same molecular pathway. The explanation of these phenotypes place ABCC6 as an upstream regulator of a purinergic pathway (ABCC6 → ENPP1 → CD73 → TNAP) that notably inhibits mineralization by maintaining a physiological Pi/PPi ratio in connective tissues. Based on a review of the literature and our recent experimental data, we suggest that PXE (and GACI/CALJA) be considered as an authentic “purinergic disease”. In this article, we recapitulate the pathobiology of PXE and review molecular and physiological data showing that, beyond PPi deficiency and ectopic calcification, PXE is associated with wide and complex alterations of purinergic systems. Finally, we speculate on the future prospects regarding purinergic signaling and other aspects of this disease. Full article
(This article belongs to the Special Issue Recent Advances in Vascular Calcification)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-2
Back to TopTop