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Molecular and Vascular Biology: From Pathophysiology to Therapy
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Molecular and Vascular Biology: From Pathophysiology to Therapy

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: 20 October 2024 | Viewed by 513

Special Issue Editor

Prof. Dr. Cristina Belizna

E-Mail Website
Guest Editor
Vascular and Coagulation Department, University Hospital Angers, 49100 Angers, France
Interests: antiphospholipid syndrome; OMICS; immune; autoimmune; rheumatology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to kindly invite you to contribute your research to the Special Issue: “Molecular and Vascular Biology: From Pathophysiology to Therapy”.

This Special Issue aims to provide insight into the basic mechanisms of vascular pathophysiologic processes like angiogenesis, atherosclerosis, thrombosis, vasculitis, and their clinical consequences. There is an expected focus on various fields such as the investigation of signal transduction mechanisms, the discovery of vessel wall disease markers, the identification and characterization of the cells that regulate immune-mediated diseases, alongside others. Additionally, there will be a particular focus on known and emerging therapeutics.

As the Guest Editor of this Special Issue, I would like to invite you to share your research with us as this will undoubtedly contribute to important advances in the area of molecular and vascular biology.

Prof. Dr. Cristina Belizna
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. 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 biology
  • angiogenesis
  • atherosclerosis
  • thrombosis
  • vasculitis

Published Papers (1 paper)

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Research

15 pages, 4388 KiB  
Article
Paricalcitol Has a Potent Anti-Inflammatory Effect in Rat Endothelial Denudation-Induced Intimal Hyperplasia
by Ciro Baeza, Arancha Pintor-Chocano, Susana Carrasco, Ana Sanz, Alberto Ortiz and Maria Dolores Sanchez-Niño
Int. J. Mol. Sci. 2024, 25(9), 4814; https://doi.org/10.3390/ijms25094814 - 28 Apr 2024
Viewed by 342
Abstract
Neointimal hyperplasia is the main cause of vascular graft failure in the medium term. Vitamin D receptor activation modulates the biology of vascular smooth muscle cells and has been reported to protect from neointimal hyperplasia following endothelial injury. However, the molecular mechanisms are [...] Read more.
Neointimal hyperplasia is the main cause of vascular graft failure in the medium term. Vitamin D receptor activation modulates the biology of vascular smooth muscle cells and has been reported to protect from neointimal hyperplasia following endothelial injury. However, the molecular mechanisms are poorly understood. We have now explored the impact of the selective vitamin D receptor activator, paricalcitol, on neointimal hyperplasia, following guidewire-induced endothelial cell injury in rats, and we have assessed the impact of paricalcitol or vehicle on the expression of key cell stress factors. Guidewire-induced endothelial cell injury caused neointimal hyperplasia and luminal stenosis and upregulated the expression of the growth factor growth/differentiation factor-15 (GDF-15), the cytokine receptor CD74, NFκB-inducing kinase (NIK, an upstream regulator of the proinflammatory transcription factor NFκB) and the chemokine monocyte chemoattractant protein-1 (MCP-1/CCL2). Immunohistochemistry confirmed the increased expression of the cellular proteins CD74 and NIK. Paricalcitol (administered in doses of 750 ng/kg of body weight, every other day) had a non-significant impact on neointimal hyperplasia and luminal stenosis. However, it significantly decreased GDF-15, CD74, NIK and MCP-1/CCL2 mRNA expression, which in paricalcitol-injured arteries remained within the levels found in control vehicle sham arteries. In conclusion, paricalcitol had a dramatic effect, suppressing the stress response to guidewire-induced endothelial cell injury, despite a limited impact on neointimal hyperplasia and luminal stenosis. This observation identifies novel molecular targets of paricalcitol in the vascular system, whose differential expression cannot be justified as a consequence of improved tissue injury. Full article
(This article belongs to the Special Issue Molecular and Vascular Biology: From Pathophysiology to Therapy)
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