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Biomedicines
Special Issues
Vascular Diseases and Therapeutics
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Vascular Diseases and Therapeutics

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 7635

Special Issue Editor

Dr. Hanna Mannell

E-Mail Website1 Website2
Guest Editor
Department of Physiology, Institute of Theoretical Medicine, Medical Faculty, University of Augsburg, Universitätsstr. 2, 86159 Augsburg, Germany
Interests: endothelial cells; vascular physiology; vascular; inflammation; nanomedicine; therapeutic targets for cardiovascular disease; hypoxia

Special Issue Information

Dear Colleagues,

Vascular diseases (VDs) encompass disorders, such as cardiovascular diseases, vasculitis, blood clotting disorders and thrombosis, and involve several processes, such as vascular inflammation, angiogenesis and vascular remodeling. Thus, several cellular systems, such as endothelial cells, platelets, immune cells, fibroblasts and vascular smooth muscle cells, play important roles in the development and progression of vascular diseases. Understanding complex mechanisms behind these events and the contribution of different vascular cells and factors is important for the identification and development of new therapeutic targets and strategies for the treatment of VDs. Moreover, the investigation of further mechanisms of action of therapeutics may open up new treatment areas.

Finally, several drugs and drug-drug interactions show adverse drug events (ADE) involving the vascular system, such as cardiotoxicity. New tools for early detection, prevention or monitoring of (cardio)vascular ADE are, thus, needed.

This Special Issue aims to cover new research on mechanisms of VDs; the identification of new potential therapeutic targets and treatment strategies; further or new mechanisms of approved substances within the field of vascular medicine; and research on (cardio)vascular ADE and welcomes original research and review articles in these areas.

Dr. Hanna Mannell
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. Biomedicines 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 2600 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

  • cardiovascular diseases
  • blood clotting disorders
  • thrombosis
  • vasculitis
  • atherosclerosis
  • vascular cells
  • vascular inflammation
  • therapeutic targets and therapies in vascular disease
  • (cardio) vascular adverse drug events
  • cardiotoxicity

Published Papers (4 papers)

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Research

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12 pages, 871 KiB  
Article
Residual Aneurysmal Sac Shrinkage Post-Endovascular Aneurysm Repair: The Role of Preoperative Inflammatory Markers
by Edoardo Pasqui, Gianmarco de Donato, Cecilia Molino, Mustafa Abu Leil, Manfredi Giuseppe Anzaldi, Giuseppe Galzerano and Giancarlo Palasciano
Biomedicines 2023, 11(7), 1920; https://doi.org/10.3390/biomedicines11071920 - 6 Jul 2023
Cited by 3 | Viewed by 1116
Abstract
Introduction: In this study, we evaluated the role of preoperative inflammatory markers as Neutrophil-to-Lymphocyte (NLR) and Platelet-to-Lymphocyte (PLR) ratios in relation to post-endovascular aneurysm repair (EVAR) sac shrinkage, which is known to be an important factor for abdominal aortic aneurysm (AAA) healing. Methods: [...] Read more.
Introduction: In this study, we evaluated the role of preoperative inflammatory markers as Neutrophil-to-Lymphocyte (NLR) and Platelet-to-Lymphocyte (PLR) ratios in relation to post-endovascular aneurysm repair (EVAR) sac shrinkage, which is known to be an important factor for abdominal aortic aneurysm (AAA) healing. Methods: This was a single-center retrospective observational study. All patients who underwent the EVAR procedure from January 2017 to December 2020 were eligible for this study. Pre-operative blood samples of all patients admitted were used to calculate NLR and PLR. Sac shrinkage was defined as a decrease of ≥5 mm in the maximal sac diameter. The optimal NLR and PLR cut-offs for aneurysmal sac shrinkage were obtained from ROC curves. Stepwise multivariate analysis was performed in order to identify independent risk and protective factors for the absence of AAA shrinkage. Kaplan–Meier curves were used to evaluate survival rates with respect to the AAA shrinkage. Results: A total of 184 patients were finally enrolled. The mean age was 75.8 ± 8.3 years, and 85.9% were male (158/184). At a mean follow-up of 43 ± 18 months, sac shrinkage was registered in 107 patients (58.1%). No-shrinking AAA patients were more likely to be older, to have a higher level of NLR and PLR, and be an active smoker. Kaplan–Meier curves highlighted a higher rate of survival for shrinking AAA patients with respect to their counterparts (p < 0.03). Multivariate analysis outlined active smoking and NLR as independent risk factors for no-shrinking AAA. Conclusions: Inflammation emerged as a possible causative factor for no-shrinking AAA, playing a role in aneurysmal sac remodeling. This study revealed that inflammatory biomarkers, such as NLR and PLR, can be used as a preoperative index of AAA sac behavior after EVAR procedures. Full article
(This article belongs to the Special Issue Vascular Diseases and Therapeutics)
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11 pages, 1713 KiB  
Article
The Effects of the Levosimendan Metabolites OR-1855 and OR-1896 on Endothelial Pro-Inflammatory Responses
by Hannah Kipka, Rebecca Schaflinger, Roland Tomasi, Kristin Pogoda and Hanna Mannell
Biomedicines 2023, 11(3), 918; https://doi.org/10.3390/biomedicines11030918 - 16 Mar 2023
Cited by 2 | Viewed by 1488
Abstract
The calcium sensitizer levosimendan is used for the treatment of acute decompensated heart failure. A small portion (4–7%) of levosimendan is metabolized to the pharmacologically active metabolite OR-1896 via the inactive intermediate OR-1855. In addition, levosimendan has been shown to exert positive effects [...] Read more.
The calcium sensitizer levosimendan is used for the treatment of acute decompensated heart failure. A small portion (4–7%) of levosimendan is metabolized to the pharmacologically active metabolite OR-1896 via the inactive intermediate OR-1855. In addition, levosimendan has been shown to exert positive effects on the endothelium in vitro antagonizing vascular dysfunction and inflammation. However, the function of the levosimendan metabolites within this context is still unknown. In this study, we thus investigated the impact of the metabolites OR-1896 and OR-1855 on endothelial inflammatory processes in vitro. We observed a reduction of IL-1β-dependent endothelial adhesion molecule ICAM-1 and VCAM-1 as well as interleukin (IL) -6 expression upon levosimendan treatment but not after treatment with OR-1855 or OR-1896, as assessed by western blotting, flow cytometry, and qRT-PCR. Instead, the metabolites impaired IL-1β-induced ROS formation via inactivation of the MAPK p38, ERK1/2, and JNK. Our results suggest that the levosimendan metabolites OR-1896 and OR-1855 have certain anti-inflammatory properties, partly other than levosimendan. Importantly, they additionally show that the intermediate metabolite OR-1855 does, in fact, have pharmacological effects in the endothelium. This is interesting, as the metabolites are responsible for the long-term therapeutic effects of levosimendan, and heart failure is associated with vascular dysfunction and inflammation. Full article
(This article belongs to the Special Issue Vascular Diseases and Therapeutics)
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10 pages, 605 KiB  
Article
The Clinical Utility of D-Dimer and Prothrombin Fragment (F1+2) for Peripheral Artery Disease: A Prospective Study
by Sara Arfan, Abdelrahman Zamzam, Muzammil H. Syed, Shubha Jain, Niousha Jahanpour, Rawand Abdin and Mohammad Qadura
Biomedicines 2022, 10(4), 878; https://doi.org/10.3390/biomedicines10040878 - 11 Apr 2022
Cited by 3 | Viewed by 2171
Abstract
D-dimer and prothrombin fragment (F1+2) levels are elevated in patients with peripheral artery disease (PAD). We examined their prognostic potential in predicting decreasing ABI and major adverse limb events (MALE). A total of 206 patients were recruited from St. Michael’s Hospital and followed [...] Read more.
D-dimer and prothrombin fragment (F1+2) levels are elevated in patients with peripheral artery disease (PAD). We examined their prognostic potential in predicting decreasing ABI and major adverse limb events (MALE). A total of 206 patients were recruited from St. Michael’s Hospital and followed for two years. Baseline plasma concentrations of D-dimer and F1+2 were recorded. Pearson’s correlation was used to assess the correlation between the biomarkers and ABI at year 2. During follow-up, multivariable Cox proportional hazard analysis was performed to investigate their role in predicting decreasing ABI (defined as change in ABI > −0.15) and MALE (defined as the need for arterial intervention or major limb amputation). Cumulative survival was assessed using Kaplan–Meier analysis. Baseline D-dimer and F1+2 levels were elevated in PAD patients (median (IQR) 1.34 (0.80–2.20) for D-dimer and 3.60 (2.30–4.74) for F1+2; p = 0.001) compared to non-PAD controls (median (IQR) 0.69 (0.29–1.20) for D-dimer and 1.84 (1.17–3.09) for F1+2; p = 0.001). Both markers were negatively correlated with ABI at year 2 (r = −0.231 for D-dimer, r = −0.49 for F1+2; p = 0.001). Cox analysis demonstrated F1+2 and D-dimer to be independent predictors of PAD status (HR = 1.27, 95% CI = 1.15–1.54; p = 0.013 for D-dimer and HR = 1.28, 95% CI = 1.14–1.58; p = 0.019 for F1+2). Elevated baseline concentrations of D-dimer and F1+2 were associated with high incidence of decreasing ABI and 1- and 2-year event-free survival (62% and 86%, respectively). Combined analysis of D-dimer and F1+2 provides important prognostic information that facilitates risk stratification for future disease progression and MALE outcomes in patients with PAD. Full article
(This article belongs to the Special Issue Vascular Diseases and Therapeutics)
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Review

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9 pages, 712 KiB  
Review
The Role of Fatty Acid Binding Protein 3 in Cardiovascular Diseases
by Ben Li, Muzammil H. Syed, Hamzah Khan, Krishna K. Singh and Mohammad Qadura
Biomedicines 2022, 10(9), 2283; https://doi.org/10.3390/biomedicines10092283 - 14 Sep 2022
Cited by 3 | Viewed by 1954
Abstract
Fatty acid binding proteins (FABPs) are proteins found in the cytosol that contribute to disorders related to the cardiovascular system, including atherosclerosis and metabolic syndrome. Functionally, FABPs serve as intracellular lipid chaperones, interacting with hydrophobic ligands and mediating their transportation to sites of [...] Read more.
Fatty acid binding proteins (FABPs) are proteins found in the cytosol that contribute to disorders related to the cardiovascular system, including atherosclerosis and metabolic syndrome. Functionally, FABPs serve as intracellular lipid chaperones, interacting with hydrophobic ligands and mediating their transportation to sites of lipid metabolism. To date, nine unique members of the FABP family (FABP 1–9) have been identified and classified according to the tissue in which they are most highly expressed. In the literature, FABP3 has been shown to be a promising clinical biomarker for coronary and peripheral artery disease. Given the rising incidence of cardiovascular disease and its associated morbidity/mortality, identifying biomarkers for early diagnosis and treatment is critical. In this review, we highlight key discoveries and recent studies on the role of FABP3 in cardiovascular disorders, with a particular focus on its clinical relevance as a biomarker for peripheral artery disease. Full article
(This article belongs to the Special Issue Vascular Diseases and Therapeutics)
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