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Biomedicines
Special Issues
Inflammatory Signaling in Vascular Endothelial Cells
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Inflammatory Signaling in Vascular Endothelial Cells

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cell Biology and Pathology".

Deadline for manuscript submissions: 31 July 2025 | Viewed by 1305

Special Issue Editor

Dr. Sanguk Yun

E-Mail Website
Guest Editor
Department of Medical Biotechnology, College of Bio Nano Information Technology (BNIT), Inje University, Gimhae, Republic of Korea
Interests: vascular inflammation and atherosclerosis; extracellular matrix (ECM) remodeling; ECM/integrin-dependent endothelial signaling and phenotype; fluid shear stress-dependent endothelial mechanotransduction

Special Issue Information

Dear Colleagues,

Endothelial cells lining the innermost layer of vasculatures actively participate in homeostasis maintenance in healthy individuals and remodeling processes in development or pathological conditions. These cells are exposed to and respond to blood flow, regulate blood vessel dilation, and promote barrier function, protecting surrounding tissues from fluid leakage or pathogen infiltration. Endothelial cells are part of immune systems and contribute to host defenses by actively participating in inflammation via recruiting immune cells such as monocytes and T-cells. This endothelial inflammation is tightly controlled by mechanisms such as laminar blood flow-induced KLF2 signaling. However, sterile endothelial inflammation involving the key inflammatory mediators NFkB or Yap, triggered by many different humoral or mechanical factors, often leads to various vascular diseases including atherosclerosis, aortic aneurysms, and pulmonary arterial hypertension. The aim of this Special Issue is to provide readers updated research on endothelial function in vascular inflammatory diseases in the form of reviews and novel research articles. The issue will cover various topics related to vascular inflammation, including but not limited to:

  • Mechanism of endothelial inflammatory signaling;
  • Function of endothelial cells and their inflammatory signaling in diseases;
  • Endothelial phenotypes and plasticity in inflammatory diseases;
  • Endothelial inflammation regulated by metabolic pathways;
  • Endothelial mechanotransduction and inflammation.

Dr. Sanguk Yun
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

  • vascular inflammation
  • endothelial cells
  • endothelial dysfunction
  • vascular diseases
  • endothelial phenotypes

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Published Papers (1 paper)

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Research

10 pages, 757 KiB  
Article
Angiopoietin II in Critically Ill Septic Patients: A Post Hoc Analysis of the DRAK Study
by Veronika Bucher, Helen Graf, Johannes Zander, Uwe Liebchen, Danilo Hackner, Caroline Gräfe, Martin Bender, Michael Zoller and Christina Scharf
Biomedicines 2024, 12(11), 2436; https://doi.org/10.3390/biomedicines12112436 - 23 Oct 2024
Viewed by 971
Abstract
Introduction: Angiopoietin II (Ang-II) plays a pivotal role in the development of microcirculatory dysfunction as it provokes endothelial barrier disruption in patients with sepsis or septic shock. In particular, those with acute kidney injury show high Ang-II concentrations. So far, it is unclear [...] Read more.
Introduction: Angiopoietin II (Ang-II) plays a pivotal role in the development of microcirculatory dysfunction as it provokes endothelial barrier disruption in patients with sepsis or septic shock. In particular, those with acute kidney injury show high Ang-II concentrations. So far, it is unclear which covariates influence Ang-II concentration in the early phase of sepsis, especially if extracorporeal therapies also do. Methods: Ang-II concentrations were measured in 171 patients with sepsis after the first day of antibiotic treatment between 03/2013 and 01/2015. Ang-II was correlated with potential influencing factors (Spearman correlation). A multivariate model was established including the significant correlating parameters. The Mann–Whitney U test and the Kruskal–Wallis test were used to detect significant differences in Ang-II concentration. Results: The median Ang-II concentration was 8015 pg/mL (interquartile range (IQR): 5024–14,185). A total of forty patients were treated with kidney replacement therapy (KRT) and 20 were supported by venovenous extracorporeal membrane oxygenation (vv-ECMO). Sequential organ failure assessment (SOFA) score (r = 0.541), creatinine clearance (r = −0.467), urinary output (r = −0.289), interleukin (IL)-6 (r = 0.529), C-reactive protein (CRP) (r = 0.241), platelet count (r = −0.419), bilirubin (r = 0.565), lactate (r = 0.322), KRT (r = 0.451), and fluid balance (r = 0.373) significantly correlated with Ang-II concentration and were included in the multivariate model. There, creatinine clearance (p < 0.01, b = −26.3, 95% confidence interval (CI) −41.8–−10.8), fluid balance (p = 0.002, b = 0.92, 95% CI 0.33–1.51), and CRP (p = 0.004, b = 127.6, 95% CI 41.6–213.7) were associated with Ang-II concentration. Furthermore, patients with KRT (median: 15,219 pg/mL, IQR: 10,548–20,270) had significantly (p < 0.01) higher Ang-II concentrations than those with vv-ECMO support (median: 6412 pg/mL, IQR: 5246–10,257) or those without extracorporeal therapy (median: 7156 pg/mL, IQR: 4409–12,741). Conclusion: Increased CRP, positive fluid balance, and impaired kidney function were associated with higher Ang-II concentrations in critically ill patients in the early stage of sepsis in this post hoc analysis. In particular, patients with KRT had very high Ang-II concentrations, whereas the use of vv-ECMO was not related to higher Ang-II concentrations. The significance for clinical practice should be clarified by a prospective study with standardized measurements. Full article
(This article belongs to the Special Issue Inflammatory Signaling in Vascular Endothelial Cells)
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