Special Issue "Clinical and Biochemical Management of Chronic Venous Disease"

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Vascular Medicine".

Deadline for manuscript submissions: 29 July 2022.

Special Issue Editors

Prof. Dr. Ferdinando Mannello
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Guest Editor
Full Professor of Clinical Biochemistry and Clinical Molecular Biology, Department of Biomolecular Sciences, Section of Biochemistry and Biotechnology, Unit of Clinical Biochemistry, University Carlo Bo of Urbino, 61029 Urbino, Italy
Interests: vascular medicine; vascular biology; inflammatory biomarkers; proteolytic biomarkers; endothelium; translational research; matrix metalloproteinases; chronic venous disorders; athero-thrombotic diseases; vascular pharmacology; vascular funcxtion; metabolomics; clinical biochemistry; nutraceuticals; platelets; neutrophils; macrophages; vascular aging; laboratory medicine; diagnostic and laboratory errors; biomarkers in cardiovascular diseases; laboratory testing for inflammatory chronic diseases
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Raouf A. Khalil
E-Mail Website
Guest Editor
Vascular Surgery Research Laboratories, Division of Vascular and Endovascular Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA
Interests: chronic venous disease; clinical management; metabolomics; biochemistry; degradomics; inflammation; venous leg ulcer; healing; non-healing; diagnosis; therapy; endothelium; hemodynamics
Prof. Dr. Joseph D. Raffetto
E-Mail Website
Guest Editor
Vascular Surgery Research Laboratories, Division of Vascular and Endovascular Surgery, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA
Interests: chronic venous disease; clinical management; metabolomics; biochemistry; degradomics; inflammation; venous leg ulcer; healing; non-healing; diagnosis; therapy; endothelium; hemodynamics
Dr. Daniela Ligi
E-Mail Website
Guest Editor
Department of Biomolecular Sciences, Section of Biochemistry and Biotechnology, Unit of Clinical Biochemistry, University Carlo Bo of Urbino, 61029 Urbino, Italy
Interests: chronic venous disease; bio-molecular approaches of wounds; inflammation; proteolysis; cytokines and growth factors; therapeutic options for improving wound healing

Special Issue Information

Dear Colleagues,

Chronic venous diseases (CVeD) of the lower limbs include different pathological events characterized by distinctive features sharing common hallmarks of hemodynamic alteration, inflammation, and proteolysis. The first step is represented by varicose veins (C-2) and the final disease is named non-healing leg ulcers (C-6), according to the international CEAP classification. CVeD affects a significant part of the populations worldwide with a prevalence up-to 15% in subjects aged over 70 years. Non-healing skin wounds represent a cause of significant disability and huge financial burden to the healthcare budget worldwide. Although great efforts have been made in characterizing early biochemical and molecular pathways during CVeD initiation and progression, discerning the biomolecular basis of healing/nonhealing processes, the exact biomolecular pathogenetic basis from C-2 to C-6 stages is not fully understood. Although several previously published histochemical, biochemical and molecular analyses, and pharmacological treatments, have indicated that the hemodynamic shear stress, pro-apoptotic and pro-inflammatory processes, coagulative events, and enhanced degradative proteolysis, may cooperate in harmful pathways leading to nonhealing ulcers, there is an urgent need to focus more attention on the importance of adequate biomolecular screening for hemodynamic stress, endothelial damage/repair, wound microenvironment, therapeutic treatments for improving CVeD management and ulcer healing. Moreover, the metabolic signature predictive of healing in venous leg ulceration may present potential translational applications for disease prognostication and development of targeted therapies. This Special Issue aims to collect insights about this complex and intricate cross talk, increasing the knowledge on both the clinical management and the pathophysiological processes of CVeD for improving the knowledge in this field, enhancing diagnosis and therapy, and translating the usefulness of investigations in vascular medicine and health sciences.

We invite experts to contribute high-quality original papers, research communications, or reviews.

Prof. Dr. Ferdinando Mannello
Prof. Dr. Raouf A. Khalil
Prof. Dr. Joseph D. Raffetto
Dr. Daniela Ligi
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 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. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly 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 2400 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

  • chronic venous disease
  • clinical management
  • metabolomics
  • biochemistry
  • degradomics
  • inflammation
  • venous leg ulcer
  • healing
  • non-healing
  • diagnosis
  • therapy
  • endothelium
  • hemodynamics

Published Papers (1 paper)

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Research

Article
The Active Isoforms of MGP Are Expressed in Healthy and Varicose Veins without Calcification
J. Clin. Med. 2021, 10(24), 5896; https://0-doi-org.brum.beds.ac.uk/10.3390/jcm10245896 - 15 Dec 2021
Viewed by 386
Abstract
Matrix Gla protein (MGP), a local inhibitor of tissue mineralization, is associated with vascular calcification. Depending on the carboxylation and phosphorylation status, MGP has active conformations, e.g., carboxylated MGP (cMGP) and phosphorylated MGP (pMGP), but also inactive conformations, e.g., uncarboxylated MGP (ucMGP) and [...] Read more.
Matrix Gla protein (MGP), a local inhibitor of tissue mineralization, is associated with vascular calcification. Depending on the carboxylation and phosphorylation status, MGP has active conformations, e.g., carboxylated MGP (cMGP) and phosphorylated MGP (pMGP), but also inactive conformations, e.g., uncarboxylated MGP (ucMGP) and dephosphorylated MGP (dpMGP). Our purpose was to assess the presence of all MGP conformations in healthy veins (HV) and varicose veins (VV), concurrently with the analysis of circulating total MGP (tMGP) before and after the surgical stripping of VV. We collected samples from the great saphenous vein, considered as control group, and tissue from VV, designated as VV group. Plasma levels of tMGP were significantly decreased after the surgical removal of the VV (before 59.5 ± 17.2 vs. after 38.1 ± 11.3, p < 0.001). By using immunohistochemistry staining, we identified local cMGP and pMGP in the control and VV groups, both without calcification, while ucMGP and dpMGP were absent. cMGP was observed in the nucleus and cytoplasm and pMGP in the nucleus of cells belonging to the tunica media, tunica intima and vasa vasorum. Therefore, the active conformations of MGP (cMGP and pMGP) are prevalent in HV and VV without calcification, affirming their anti-calcifying role in veins. Full article
(This article belongs to the Special Issue Clinical and Biochemical Management of Chronic Venous Disease)
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