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IJMS
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Mechanisms of Vascular Calcification 2.0
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Mechanisms of Vascular Calcification 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 2711

Special Issue Editors

Prof. Dr. Jakob Voelkl

E-Mail Website
Guest Editor
Institute for Physiology, Johannes Kepler University Linz, 4040 Linz, Austria
Interests: vascular calcification; vascular smooth muscle cells; phosphate homeostasis; chronic kidney disease; vascular stiffness and fibrosis; cardiac remodeling
Special Issues, Collections and Topics in MDPI journals
Dr. Mirjam Schuchardt

E-Mail Website
Guest Editor
Department of Nephrology, Charité-Universitätsmedizin Berlin, 13353 Berlin, Germany
Interests: vascular calcification; vascular senescence
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Ectopic calcification in cardiovascular tissue is a common phenomenon closely connected with cardiovascular mortality. However, the underlying mechanisms are complex and currently no widely available treatment is available to prevent the development and progression of ectopic calcifications.

Under physiological conditions, the ectopic deposition of calcium and phosphate is regulated by a fine-tuned system of local and circulating calcification inhibitors. Various pathological conditions can shift this balance, thereby resulting in “mineral stress”, ultimately leading to ectopic calcifications as a consequence of active mineralization processes. Various stimuli may induce the reprogramming of vascular smooth muscle cells, fibroblast-like cells, endothelial cells, and other cell types into cells with pro-calcific properties. These “transdifferentiated” cells can augment ectopic mineralization using various mechanisms such as the release of calcifying vesicles, an impairment of calcification inhibitors or matrix remodelling. Inflammatory mediators are recognized for activating intracellular pathways, which promote calcific processes. However, the complex and diverse mechanisms participating in various forms of ectopic calcification are still not completely understood. Advancing research in this field is needed to establish new therapeutic concepts.

After a successful first Special Issue of IJMS, we cordially invite you again to submit research works on “Mechanisms of Cardiovascular Calcification". This call is aimed to encourage submissions of focused reviews and original work of relevant pre-clinical and clinical studies regarding the development, progression and consequences of ectopic cardiovascular calcifications as well as novel methodological approaches.

Prof. Dr. Jakob Voelkl
Dr. Mirjam Schuchardt
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 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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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
  • valvular calcification
  • vascular smooth muscle cells
  • endothelial cells
  • procalcific signaling molecules
  • calcification inhibitors
  • phosphate/calcium homeostasis
  • pro-/anticalcific signaling pathways
  • regulation of calcium–phosphate deposition
  • consequences of cardiovascular calcification

Published Papers (2 papers)

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Research

12 pages, 3377 KiB  
Article
Leucine-Rich Alpha-2 Glycoprotein 1 Accumulates in Complicated Atherosclerosis and Promotes Calcification
by Lucile Grzesiak, Ana Amaya-Garrido, Guylène Feuillet, Nicole Malet, Audrey Swiader, Marie-Kerguelen Sarthou, Amandine Wahart, Damien Ramel, Stéphanie Gayral, Joost Peter Schanstra, Julie Klein and Muriel Laffargue
Int. J. Mol. Sci. 2023, 24(22), 16537; https://doi.org/10.3390/ijms242216537 - 20 Nov 2023
Viewed by 948
Abstract
Atherosclerosis is the primary cause of cardiovascular disease. The development of plaque complications, such as calcification and neo-angiogenesis, strongly impacts plaque stability and is a good predictor of mortality in patients with atherosclerosis. Despite well-known risk factors of plaque complications, such as diabetes [...] Read more.
Atherosclerosis is the primary cause of cardiovascular disease. The development of plaque complications, such as calcification and neo-angiogenesis, strongly impacts plaque stability and is a good predictor of mortality in patients with atherosclerosis. Despite well-known risk factors of plaque complications, such as diabetes mellitus and chronic kidney disease, the mechanisms involved are not fully understood. We and others have identified that the concentration of circulating leucine-rich α-2 glycoprotein 1 (LRG1) was increased in diabetic and chronic kidney disease patients. Using apolipoprotein E knockout mice (ApoE−/−) (fed with Western diet) that developed advanced atherosclerosis and using human carotid endarterectomy, we showed that LRG1 accumulated into an atherosclerotic plaque, preferentially in calcified areas. We then investigated the possible origin of LRG1 and its functions on vascular cells and found that LRG1 expression was specifically enhanced in endothelial cells via inflammatory mediators and not in vascular smooth muscle cells (VSMC). Moreover, we identified that LRG1 was able to induce calcification and SMAD1/5-signaling pathways in VSMC. In conclusion, our results identified for the first time that LRG1 is a direct contributor to vascular calcification and suggest a role of this molecule in the development of plaque complications in patients with atherosclerosis. Full article
(This article belongs to the Special Issue Mechanisms of Vascular Calcification 2.0)
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9 pages, 3195 KiB  
Communication
GSK3β Inhibition Reduced Vascular Calcification in Ins2Akita/+ Mice
by Kristina I. Boström, Xiaojing Qiao, Yan Zhao, Xiuju Wu, Li Zhang, Jocelyn A. Ma, Jaden Ji, Xinjiang Cai and Yucheng Yao
Int. J. Mol. Sci. 2023, 24(6), 5971; https://doi.org/10.3390/ijms24065971 - 22 Mar 2023
Cited by 2 | Viewed by 1262
Abstract
Endothelial–mesenchymal transition (EndMT) drives the endothelium to contribute to vascular calcification in diabetes mellitus. In our previous study, we showed that glycogen synthase kinase-3β (GSK3β) inhibition induces β-catenin and reduces mothers against DPP homolog 1 (SMAD1) to direct osteoblast-like cells toward endothelial lineage, [...] Read more.
Endothelial–mesenchymal transition (EndMT) drives the endothelium to contribute to vascular calcification in diabetes mellitus. In our previous study, we showed that glycogen synthase kinase-3β (GSK3β) inhibition induces β-catenin and reduces mothers against DPP homolog 1 (SMAD1) to direct osteoblast-like cells toward endothelial lineage, thereby reducing vascular calcification in Matrix Gla Protein (Mgp) deficiency. Here, we report that GSK3β inhibition reduces vascular calcification in diabetic Ins2Akita/wt mice. Cell lineage tracing reveals that GSK3β inhibition redirects endothelial cell (EC)-derived osteoblast-like cells back to endothelial lineage in the diabetic endothelium of Ins2Akita/wt mice. We also find that the alterations in β-catenin and SMAD1 by GSK3β inhibition in the aortic endothelium of diabetic Ins2Akita/wt mice are similar to Mgp−/− mice. Together, our results suggest that GSK3β inhibition reduces vascular calcification in diabetic arteries through a similar mechanism to that in Mgp−/− mice. Full article
(This article belongs to the Special Issue Mechanisms of Vascular Calcification 2.0)
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