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New Insights into Endothelial Injury
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New Insights into Endothelial Injury

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: closed (31 January 2024) | Viewed by 15318

Special Issue Editors

Dr. Eleni Gavriilaki

E-Mail Website
Guest Editor
Second Propedeutic Department of Internal Medicine, Hippocration Hospital, Aristotle University of Thessaloniki, 54642 Thessaloniki, Greece
Interests: hematologic malignancies; thrombosis; complement; cellular therapy; lymphoma; myeloma; COVID-19
Special Issues, Collections and Topics in MDPI journals
Dr. Panagiota Anyfanti

E-Mail Website
Guest Editor
Third Department of Internal Medicine, Papageorgiou Hospital, Aristotle University of Thessaloniki, 56403 Thessaloniki, Greece
Interests: vascular pathology; endothelial dysfunction; hypertension; cardiovascular diseases; chronic inflammation; autoimmune rheumatic disorders
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Since the endothelium was first studied in the 1950s, endothelial injury has been recognized as a major pathophysiological process in the ever-expanding list of endothelial injury syndromes. Endothelial injury involves structural and functional alterations of the endothelium—which is considered a dynamic organ with multiple functions—that lead to vessel wall disease. In the cardiovascular field, the vicious cycle of endothelial injury and regeneration has been well described as a cause and consequence of cardiovascular disease. Beyond this, endothelial injury is associated with an expanding variety of clinical settings, including hematological disorders such as hematopoietic cell transplantation, chronic immune-mediated inflammatory diseases, toxic syndromes, and new entities such as coronavirus disease-2019 (COVID-19).

The mechanism of endothelial injury involves a variety of predisposing factors, mainly inflammation and oxidative stress, but also factors such as physical stimulation, toxins, concurrent related diseases, and aging. However, the exact mechanism of endothelial injury is not fully understood. This Special Issue will provide new insights into the molecular mechanisms, diagnosis, and treatment of endothelial injury and related syndromes.

More specifically, the aim is to collect original studies and comprehensive reviews on this research topic focused at the molecular level. Topics may include (but are not limited to) the study of endothelial injury in the following areas:

  • Cardiovascular diseases
  • Hematological disorders including hematopoietic cell transplantation
  • Chronic inflammatory disorders, including autoimmune rheumatic diseases
  • Novel entities recognized as endotheliopathies, such as COVID-19

Dr. Eleni Gavriilaki
Dr. Panagiota Anyfanti
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 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

  • endothelial injury
  • endotheliopathies
  • endothelial dysfunction
  • COVID-19
  • hematological disorders
  • cardiovascular disorders
  • hematopoietic cell transplantations
  • autoimmune diseases

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Published Papers (6 papers)

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Research

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22 pages, 5902 KiB  
Article
The Specific Molecular Changes Induced by Diabetic Conditions in Valvular Endothelial Cells and upon Their Interactions with Monocytes Contribute to Endothelial Dysfunction
by Monica Madalina Tucureanu, Letitia Ciortan, Razvan Daniel Macarie, Andreea Cristina Mihaila, Ionel Droc, Elena Butoi and Ileana Manduteanu
Int. J. Mol. Sci. 2024, 25(5), 3048; https://doi.org/10.3390/ijms25053048 - 6 Mar 2024
Viewed by 1248
Abstract
Aortic valve disease (AVD) represents a global public health challenge. Research indicates a higher prevalence of diabetes in AVD patients, accelerating disease advancement. Although the specific mechanisms linking diabetes to valve dysfunction remain unclear, alterations of valvular endothelial cells (VECs) homeostasis due to [...] Read more.
Aortic valve disease (AVD) represents a global public health challenge. Research indicates a higher prevalence of diabetes in AVD patients, accelerating disease advancement. Although the specific mechanisms linking diabetes to valve dysfunction remain unclear, alterations of valvular endothelial cells (VECs) homeostasis due to high glucose (HG) or their crosstalk with monocytes play pivotal roles. The aim of this study was to determine the molecular signatures of VECs in HG and upon their interaction with monocytes in normal (NG) or high glucose conditions and to propose novel mechanisms underlying valvular dysfunction in diabetes. VECs and THP-1 monocytes cultured in NG/HG conditions were used. The RNAseq analysis revealed transcriptomic changes in VECs, in processes related to cytoskeleton regulation, focal adhesions, cellular junctions, and cell adhesion. Key molecules were validated by qPCR, Western blot, and immunofluorescence assays. The alterations in cytoskeleton and intercellular junctions impacted VEC function, leading to changes in VECs adherence to extracellular matrix, endothelial permeability, monocyte adhesion, and transmigration. The findings uncover new molecular mechanisms of VEC dysfunction in HG conditions and upon their interaction with monocytes in NG/HG conditions and may help to understand mechanisms of valvular dysfunction in diabetes and to develop novel therapeutic strategies in AVD. Full article
(This article belongs to the Special Issue New Insights into Endothelial Injury)
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14 pages, 3739 KiB  
Article
Influence of Race and High Laminar Shear Stress on TNFR1 Signaling in Endothelial Cells
by Maitha Aldokhayyil, Dulce H. Gomez, Marc D. Cook, Andreas N. Kavazis, Michael D. Roberts, Thangiah Geetha and Michael D. Brown
Int. J. Mol. Sci. 2023, 24(19), 14723; https://doi.org/10.3390/ijms241914723 - 29 Sep 2023
Cited by 1 | Viewed by 1571
Abstract
Tumor necrosis factor (TNF) binding to endothelial TNF receptor-I (TNFR-I) facilitates monocyte recruitment and chronic inflammation, leading to the development of atherosclerosis. In vitro data show a heightened inflammatory response and atherogenic potential in endothelial cells (ECs) from African American (AA) donors. High [...] Read more.
Tumor necrosis factor (TNF) binding to endothelial TNF receptor-I (TNFR-I) facilitates monocyte recruitment and chronic inflammation, leading to the development of atherosclerosis. In vitro data show a heightened inflammatory response and atherogenic potential in endothelial cells (ECs) from African American (AA) donors. High laminar shear stress (HSS) can mitigate some aspects of racial differences in endothelial function at the cellular level. We examined possible racial differences in TNF-induced monocyte adhesion and TNFR1 signaling complex expression/activity, along with the effects of HSS. Tohoku Hospital Pediatrics-1 (THP-1) monocytes were used in a co-culture system with human umbilical vein ECs (HUVECs) from Caucasian American (CA) and AA donors to examine racial differences in monocyte adhesion. An in vitro exercise mimetic model was applied to investigate the potential modulatory effect of HSS. THP-1 adherence to ECs and TNF-induced nuclear factor kappa B (NF-κB) DNA binding were elevated in AA ECs compared to CA ECs, but not significantly. We report no significant racial differences in the expression of the TNFR-I signaling complex. Application of HSS significantly increased the expression and shedding of TNFR-I and the expression of TRAF3, and decreased the expression of TRAF5 in both groups. Our data does not support TNF-induced NF-κB activation as a potential mediator of racial disparity in this model. Other pathways and associated factors activated by the TNFR1 signaling complex are recommended targets for future research. Full article
(This article belongs to the Special Issue New Insights into Endothelial Injury)
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12 pages, 1961 KiB  
Article
Endothelial Injury Syndromes after Allogeneic Hematopoietic Stem Cell Transplantation: Angiopetin-2 as a Novel Predictor of the Outcome and the Role of Functional Autoantibodies against Angiotensin II Type 1 and Endothelin A Receptor
by Dionysios Vythoulkas, Ioanna Lazana, Christos Kroupis, Eleni Gavriilaki, Ioannis Konstantellos, Zoi Bousiou, Spiros Chondropoulos, Marianna Griniezaki, Anna Vardi, Konstantinos Gkirkas, Aggeliki Karagiannidou, Ioannis Batsis, Maria Stamouli, Ioanna Sakellari and Panagiotis Tsirigotis
Int. J. Mol. Sci. 2023, 24(8), 6960; https://doi.org/10.3390/ijms24086960 - 9 Apr 2023
Cited by 2 | Viewed by 2096
Abstract
Transplant-associated thrombotic microangiopathy (TMA) occurs in a significant percentage of patients after allogeneic stem cell transplantation (allo-SCT) and is associated with significant morbidity and mortality. The aim of the present study was to examine the association of serum angiopoetin-2 (Ang2) levels and the [...] Read more.
Transplant-associated thrombotic microangiopathy (TMA) occurs in a significant percentage of patients after allogeneic stem cell transplantation (allo-SCT) and is associated with significant morbidity and mortality. The aim of the present study was to examine the association of serum angiopoetin-2 (Ang2) levels and the presence of antibodies against angiotensin II type 1 (AT1R) and ndothelin A Recreptor (ETAR) with the outcome of patients with TMA and/or graft-versus-host disease (GVHD) after allo-SCT. Analysis of our data showed that elevated serum Ang2 levels at the time of TMA diagnosis are significantly associated with increased non-relapse mortality and decreased overall survival. To our knowledge, this is the first study demonstrating an association between raised Ang2 levels and poor outcomes in patients with TMA. Antibodies against AT1R (AT1R-Abs) and ETAR (ETAR-Abs) were detected in 27% and 23% of the patients, respectively, but there was no association between the presence of autoantibodies and the outcome of patients with TMA. However, a significant finding was the strong positive correlation between the presence of AT1R-Abs with the occurrence of chronic fibrotic GVHD, such as scleroderma and cryptogenic organizing pneumonia, raising the possibility of the contribution of autoantibodies in the pathogenesis of fibrotic GVHD manifestations. Full article
(This article belongs to the Special Issue New Insights into Endothelial Injury)
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15 pages, 2005 KiB  
Article
The Endothelial Glycocalyx as a Target of Excess Soluble Fms-like Tyrosine Kinase-1
by Annika Schulz, Carolin C. Drost, Bettina Hesse, Katrin Beul, Göran R. Boeckel, Alexander Lukasz, Hermann Pavenstädt, Marcus Brand and Giovana S. Di Marco
Int. J. Mol. Sci. 2023, 24(6), 5380; https://doi.org/10.3390/ijms24065380 - 11 Mar 2023
Cited by 3 | Viewed by 2394
Abstract
Soluble fms-like tyrosine kinase-1 (sFlt-1) is a secreted protein that binds heparan sulfate expressed on the endothelial glycocalyx (eGC). In this paper we analyze how excess sFlt-1 causes conformational changes in the eGC, leading to monocyte adhesion, a key event triggering vascular dysfunction. [...] Read more.
Soluble fms-like tyrosine kinase-1 (sFlt-1) is a secreted protein that binds heparan sulfate expressed on the endothelial glycocalyx (eGC). In this paper we analyze how excess sFlt-1 causes conformational changes in the eGC, leading to monocyte adhesion, a key event triggering vascular dysfunction. In vitro exposure of primary human umbilical vein endothelial cells to excess sFlt-1 decreased eGC height and increased stiffness as determined by atomic force microscopy (AFM). Yet, structural loss of the eGC components was not observed, as indicated by Ulex europaeus agglutinin I and wheat germ agglutinin staining. Moreover, the conformation observed under excess sFlt-1, a collapsed eGC, is flat and stiff with unchanged coverage and sustained content. Functionally, this conformation increased the endothelial adhesiveness to THP-1 monocytes by about 35%. Heparin blocked all these effects, but the vascular endothelial growth factor did not. In vivo administration of sFlt-1 in mice also resulted in the collapse of the eGC in isolated aorta analyzed ex vivo by AFM. Our findings show that excess sFlt-1 causes the collapse of the eGC and favors leukocyte adhesion. This study provides an additional mechanism of action by which sFlt-1 may cause endothelial dysfunction and injury. Full article
(This article belongs to the Special Issue New Insights into Endothelial Injury)
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Review

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18 pages, 2042 KiB  
Review
Shear Stress-Induced AMP-Activated Protein Kinase Modulation in Endothelial Cells: Its Role in Metabolic Adaptions and Cardiovascular Disease
by Philipp C. Hauger and Peter L. Hordijk
Int. J. Mol. Sci. 2024, 25(11), 6047; https://doi.org/10.3390/ijms25116047 - 31 May 2024
Cited by 7 | Viewed by 2348
Abstract
Endothelial cells (ECs) line the inner surface of all blood vessels and form a barrier that facilitates the controlled transfer of nutrients and oxygen from the circulatory system to surrounding tissues. Exposed to both laminar and turbulent blood flow, ECs are continuously subject [...] Read more.
Endothelial cells (ECs) line the inner surface of all blood vessels and form a barrier that facilitates the controlled transfer of nutrients and oxygen from the circulatory system to surrounding tissues. Exposed to both laminar and turbulent blood flow, ECs are continuously subject to differential mechanical stimulation. It has been well established that the shear stress associated with laminar flow (LF) is atheroprotective, while shear stress in areas with turbulent flow (TF) correlates with EC dysfunction. Moreover, ECs show metabolic adaptions to physiological changes, such as metabolic shifts from quiescence to a proliferative state during angiogenesis. The AMP-activated protein kinase (AMPK) is at the center of these phenomena. AMPK has a central role as a metabolic sensor in several cell types. Moreover, in ECs, AMPK is mechanosensitive, linking mechanosensation with metabolic adaptions. Finally, recent studies indicate that AMPK dysregulation is at the center of cardiovascular disease (CVD) and that pharmacological targeting of AMPK is a promising and novel strategy to treat CVDs such as atherosclerosis or ischemic injury. In this review, we summarize the current knowledge relevant to this topic, with a focus on shear stress-induced AMPK modulation and its consequences for vascular health and disease. Full article
(This article belongs to the Special Issue New Insights into Endothelial Injury)
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36 pages, 1026 KiB  
Review
Endotheliopathy in Acute COVID-19 and Long COVID
by Alice G. Vassiliou, Charikleia S. Vrettou, Chrysi Keskinidou, Ioanna Dimopoulou, Anastasia Kotanidou and Stylianos E. Orfanos
Int. J. Mol. Sci. 2023, 24(9), 8237; https://doi.org/10.3390/ijms24098237 - 4 May 2023
Cited by 31 | Viewed by 4601
Abstract
The pulmonary endothelium is a highly regulated organ that performs a wide range of functions under physiological and pathological conditions. Since endothelial dysfunction has been demonstrated to play a direct role in sepsis and acute respiratory distress syndrome, its role in COVID-19 has [...] Read more.
The pulmonary endothelium is a highly regulated organ that performs a wide range of functions under physiological and pathological conditions. Since endothelial dysfunction has been demonstrated to play a direct role in sepsis and acute respiratory distress syndrome, its role in COVID-19 has also been extensively investigated. Indeed, apart from the COVID-19-associated coagulopathy biomarkers, new biomarkers were recognised early during the pandemic, including markers of endothelial cell activation or injury. We systematically searched the literature up to 10 March 2023 for studies examining the association between acute and long COVID-19 severity and outcomes and endothelial biomarkers. Full article
(This article belongs to the Special Issue New Insights into Endothelial Injury)
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