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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 2684

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

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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 (3 papers)

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Research

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11 pages, 1035 KiB  
Article
Lactate Clearance of the Adsorber Cytosorb® in Critically Ill Patients: A Post-Hoc Analysis of the Cyto-SOLVE Trial
by Vassilissa Wustrow, Caroline Gräfe, Helen Graf, Patrick Scheiermann, Michael Paal, Michael Vogeser, Uwe Liebchen and Christina Scharf
Biomedicines 2025, 13(2), 418; https://doi.org/10.3390/biomedicines13020418 - 10 Feb 2025
Viewed by 770
Abstract
Background/Objectives: Patients with shock suffer from hyperlactatemia, which can lead to endothelial dysfunction. The use of the adsorber Cytosorb® (CS) is recommended in these patients as it may contribute to higher lactate clearance and hemodynamic stabilization. However, it is unclear whether [...] Read more.
Background/Objectives: Patients with shock suffer from hyperlactatemia, which can lead to endothelial dysfunction. The use of the adsorber Cytosorb® (CS) is recommended in these patients as it may contribute to higher lactate clearance and hemodynamic stabilization. However, it is unclear whether CS can directly adsorb lactate and can therefore increase lactate clearance. Methods: The Cyto-SOLVE trial included patients undergoing continuous kidney replacement therapy combined with CS application. Patients with a lactate concentration > 2 mmol/L and measurements of lactate pre- and post-adsorber, as well as measurements in the blood 10 min and 1, 3, 6, and 12 h after initiation were selected. Lactate clearance was calculated using the following formula: bloodflow(mL/min) × concentrationpre−post/concentrationpre. A t-test was used with the collected samples. Changes in the lactate concentration and vasopressor requirement were recorded before initiation and at the end of therapy. Results: Sixty-five lactate concentrations were measured pre- and post-CS application, as well as in patients’ blood, in a total of 14 patients (median age of 52 years, 10 males, median SAPS-II 67). There was no significant change in the lactate concentration pre- and post-CS application (mean pre-CS: 6.7 mmol/L, mean post-CS: 6.9 mmol/L, RR: −0.2, 95% confidence interval (CI): −0.4–0.1, p = 0.13, Cohen’s d: 0.90). The mean lactate clearance was −6 mL/min (standard deviation (SD): 21 mL/min), with no correlation with the initial lactate concentration or blood flow. In contrast, the mean lactate clearance measured using the dialyzer was 39 mL/min (SD: 28 mL/min). When comparing values before and after treatment, no significant change was observed in the lactate blood concentrations (mean of 9.0 vs. 8.5 mmol/L), nor in the requirement for vasopressin (median of 1.9 vs. 1.8 IE/h) or norepinephrine (mean of 2.7 vs. 2.6 mg/h). Conclusions: The adsorber CS cannot directly adsorb lactate, unlike kidney replacement therapy. Therefore, it is not suitable for achieving faster extracorporeal lactate elimination. Understanding the adsorption spectrum is of great relevance and should be considered when using CS in clinical practice. Full article
(This article belongs to the Special Issue Inflammatory Signaling in Vascular Endothelial Cells)
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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 1160
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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Review

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23 pages, 862 KiB  
Review
Multifaceted Role of Notch Signaling in Vascular Health and Diseases
by Ahsan Ali and Sanguk Yun
Biomedicines 2025, 13(4), 837; https://doi.org/10.3390/biomedicines13040837 - 31 Mar 2025
Viewed by 282
Abstract
Notch signaling is evolutionarily conserved from Drosophila to mammals and it functions as an essential modulator of vascular growth and development by directing endothelial cell specification, proliferation, migration, arteriovenous differentiation, inflammation, and apoptosis. The interplay between Notch and other signaling pathways plays a [...] Read more.
Notch signaling is evolutionarily conserved from Drosophila to mammals and it functions as an essential modulator of vascular growth and development by directing endothelial cell specification, proliferation, migration, arteriovenous differentiation, inflammation, and apoptosis. The interplay between Notch and other signaling pathways plays a homeostatic role by modulating multiple vascular functions, including permeability regulation, angiogenesis, and vascular remodeling. This review explores current knowledge on Notch signaling in vascular development, homeostasis, and disease. It also discusses recent developments in understanding how endothelial Notch signaling affects vascular inflammation via cytokines or aberrant shear stress in endothelial cells while addressing the reciprocal relationship between Notch signaling and inflammation. Full article
(This article belongs to the Special Issue Inflammatory Signaling in Vascular Endothelial Cells)
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