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Molecular Research on Endothelial Cell Injury and Repair

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: 30 August 2025 | Viewed by 691

Special Issue Editors


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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
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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,

Endothelial cells play a pivotal role in vascular homeostasis and fluid balance though a continuous “cross-talk” between the circulation and the surrounding tissues. Endothelial cell injury disturbs endothelial junctions, dysregulates vascular function and damages the homeostatic balance. The regulatory mechanisms responsible for endothelial regeneration and vascular repair are then potentiated, but they are not always effective in restoring the function of the endothelial barrier, regenerating a functional endothelium and reversing vascular damage. As a result, endothelial injury triggers several pathophysiological pathways, eventually resulting in the establishment of a continuously expanding list of diverse clinical diseases.

Despite  recent advances, a comprehensive understanding of the molecular mechanisms and signaling pathways that are responsible for endothelial injury and the regulatory mechanisms that mediate endothelial repair and vascular regeneration is lacking. This would facilitate the development of innovative treatment strategies for a wide range of systemic diseases. This Special Issue therefore welcomes the submission of articles that present new concepts and knowledge, including insights into endothelial cell injury and repair. The scope of this Special Issue includes, but is not limited to, the following topics:

  • Cardiovascular diseases;
  • Hematological disorders including hematopoietic cell transplantation;
  • Chronic inflammatory disorders including autoimmune rheumatic diseases;
  • Sepsis and acute respiratory distress syndrome;
  • Novel entities recognized as endotheliopathies, such as COVID-19.

Dr. Eleni Gavriilaki
Dr. Panagiota Anyfanti
Guest Editors

Manuscript Submission Information

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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
  • endothelial repair
  • endotheliopathies
  • endothelial dysfunction

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Published Papers (1 paper)

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22 pages, 4561 KiB  
Article
Are You a Friend or an Enemy? The Dual Action of Methylglyoxal on Brain Microvascular Endothelial Cells
by Roberta Moisă (Stoica), Călin Mircea Rusu, Antonia Teona Deftu, Mihaela Bacalum, Mihai Radu and Beatrice Mihaela Radu
Int. J. Mol. Sci. 2025, 26(11), 5104; https://doi.org/10.3390/ijms26115104 - 26 May 2025
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Abstract
Methylglyoxal is a reactive dicarbonyl intermediate in the advanced glycation end-product (AGE) pathway, and alterations in its levels have been detected in the plasma, cerebrospinal fluid, and brain parenchyma in various pathologies, particularly in diabetes. In this study, we investigate the effects of [...] Read more.
Methylglyoxal is a reactive dicarbonyl intermediate in the advanced glycation end-product (AGE) pathway, and alterations in its levels have been detected in the plasma, cerebrospinal fluid, and brain parenchyma in various pathologies, particularly in diabetes. In this study, we investigate the effects of methylglyoxal (MGO) on murine brain microvascular endothelial cells at both physiological and pathological concentrations. We evaluate molecular parameters, including reactive oxygen species (ROS) production, cytosolic calcium signaling, and ATP synthesis, as well as cellular responses such as cytoskeletal remodeling, cell migration, adhesion, and permeability, across a concentration range of 0–1000 μM. At low concentrations (below ~250 μM), MGO does not induce oxidative stress; instead, it leads to an increase in cytosolic calcium levels and ATP production. At higher concentrations, however, MGO induces significant oxidative stress, which is accompanied by a marked decrease in cell viability, particularly at concentrations exceeding 500 μM. The modulation of key functional processes, including purinergic calcium signaling, actin filament synthesis, cell migration, and adhesion, reveals a threshold concentration beyond which cellular function is impaired due to oxidative stress. Below this threshold, the observed effects appear to be mediated primarily by non-oxidative mechanisms, likely involving protein glycation. In conclusion, our results suggest a dual action of methylglyoxal on brain endothelial cells, with distinct molecular mechanisms underlying its effects at physiological versus pathological concentrations. Full article
(This article belongs to the Special Issue Molecular Research on Endothelial Cell Injury and Repair)
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