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The Molecular Basis of Vascular Pathology
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The Molecular Basis of Vascular Pathology

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: 20 September 2025 | Viewed by 1069

Special Issue Editor

Dr. Jolanta Neubauer-Geryk

E-Mail Website
Guest Editor
Clinical Physiology Unit, Medical Simulation Centre, Medical University of Gdańsk, Gdansk, Poland
Interests: endothelial dysfunction; microcirculation; macrocirculation; diabetes mellitus; cardiovascular diseases
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Vascular pathologies result from intricate interactions between multiple molecular mechanisms that culminate in the impairment and dysfunction of blood vessels. These changes occur in the endothelium, vascular smooth muscle, and extracellular matrix, as well as the immune and coagulation systems. Factors such as hypertension, hyperglycemia, high cholesterol, and smoking contribute to endothelial dysfunction, which results in increased vessel wall permeability. This facilitates the passage of lipids and other substances, initiating inflammatory processes. Pro-inflammatory cytokines and immune cells, including macrophages and T lymphocytes, drive the inflammatory process in blood vessel walls. These cells and factors can result in further vascular damage, increased proliferative processes, and the activation of smooth muscle cells, contributing to structural changes in the vessel walls. Similarly, oxidative stress plays a pivotal role in the progression of numerous vascular pathologies. This phenomenon stems from the excessive production of reactive oxygen species, which directly cause damage to the endothelium, ultimately leading to the formation of plaques that impede blood flow. Abnormal activation of the coagulation cascade can lead to the formation of clots, which may result in myocardial infarction, stroke, or pulmonary embolism.

All of the aforementioned processes contribute to the development and progression of vascular disease. A comprehensive understanding of these mechanisms is vital for the development of effective therapeutic strategies that could prevent these diseases or slow their progression.

This Special Issue of the International Journal of Molecular Sciences details the latest research on the molecular bases, early diagnosis, and treatment of vascular pathology. Titled “The Molecular Basis of Vascular Pathology”, this Special Issue welcomes in vitro and in vivo studies, as well as original research and reviews.

Dr. Jolanta Neubauer-Geryk
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. 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

  • vascular pathologies
  • blood vessels
  • dysfunction
  • vascular damage
  • blood flow
  • biomarkers
  • biomolecules
  • cytokines

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Published Papers (2 papers)

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Research

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15 pages, 10600 KiB  
Article
The Role of Hippo Signaling in Brain Arteriovenous Malformations: Molecular Insights into Post-Embolization Remodeling
by Belal Neyazi, Vanessa Magdalena Swiatek, Mohammad Ali Karimpour, Sarah Stassen, Klaus-Peter Stein, Ali Rashidi, Claudia Alexandra Dumitru and I. Erol Sandalcioglu
Int. J. Mol. Sci. 2025, 26(8), 3791; https://doi.org/10.3390/ijms26083791 - 17 Apr 2025
Viewed by 204
Abstract
Brain arteriovenous malformations (bAVMs) are complex vascular lesions with significant clinical risks. The Hippo signaling pathway, particularly its downstream effector YAP, plays a crucial role in angiogenesis and vascular remodeling. This study investigates the role of YAP and related molecular markers in bAVMs, [...] Read more.
Brain arteriovenous malformations (bAVMs) are complex vascular lesions with significant clinical risks. The Hippo signaling pathway, particularly its downstream effector YAP, plays a crucial role in angiogenesis and vascular remodeling. This study investigates the role of YAP and related molecular markers in bAVMs, focusing on the effects of embolization. Immunohistochemical analysis was conducted on tissue samples from bAVM patients (n = 127), as well as on healthy blood vessels (n = 17). YAP, HIF-1α, FGFR1, CTGF, and CYR61 expression were quantified and correlated with clinical parameters. Results: In healthy vessels, YAP exhibited nuclear localization in (sub)endothelial cells and the tunica media, while CTGF and CYR61 were detected in the cytoplasm and extracellular matrix. The expression of YAP, CTGF, and CYR61 was significantly lower in bAVM tissues. Embolized bAVMs exhibited significantly higher expression of YAP, CTGF, and CYR61 compared to non-embolized tissues, suggesting a link between embolization and pro-angiogenic signaling. Additionally, FGFR1 was upregulated in embolized tissues. These results suggest that upregulation of YAP expression via the Hippo pathway might play a key role in bAVM pathophysiology. Embolization may further promote vascular remodeling. Dysregulation of YAP and related molecules in bAVMs warrants further studies to explore potential therapeutic strategies targeting the Hippo pathway. Full article
(This article belongs to the Special Issue The Molecular Basis of Vascular Pathology)
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Review

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23 pages, 1972 KiB  
Review
A Systematic Review of Endothelial Dysfunction in Chronic Venous Disease—Inflammation, Oxidative Stress, and Shear Stress
by Hristo Abrashev, Despina Abrasheva, Nadelin Nikolov, Julian Ananiev and Ekaterina Georgieva
Int. J. Mol. Sci. 2025, 26(8), 3660; https://doi.org/10.3390/ijms26083660 - 12 Apr 2025
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Abstract
Chronic venous disease (CVD) is among the most common diseases in industrialized countries and has a significant socioeconomic impact. The diversity of clinical symptoms and manifestations of CVD pose major challenges in routine diagnosis and treatment. Despite the high prevalence and the huge [...] Read more.
Chronic venous disease (CVD) is among the most common diseases in industrialized countries and has a significant socioeconomic impact. The diversity of clinical symptoms and manifestations of CVD pose major challenges in routine diagnosis and treatment. Despite the high prevalence and the huge number of venous surgical interventions performed every day, a substantial proportion of the etiopathogenesis remains unclear. There are several widely advocated and generally valid theories of “peri-capillary fibrin cuffs” and “white cell trapping hypothesis”, which consider the role of venous reflux/obstruction, inflammation, vascular remodeling, hemodynamic changes, genetic and social risk factors. There are several specific provoking factors for the development of venous reflux: incompetence of the valve system, inflammation of the vascular wall, and venous hypertension. Over the past few years, increasing scientific data has demonstrated the link between oxidative stress, endothelial dysfunction, and vascular inflammation. High levels of oxidants and persistent inflammation can cause cumulative changes in hemodynamics, resulting in permanent and irreversible damage to the microcirculation and endothelial cells. Production of reactive oxygen species and expression of inflammatory cytokines and adhesion molecules are involved in a vicious cycle of venous wall remodeling. The interaction of ROS, and in particular, the superoxide anion radical, with nitric oxide leads to a decrease in NO bioavailability, followed by the initiation of prolonged vasoconstriction and hypoxia and impairment of vascular tone. This review addresses the role of ED, oxidative, and hemodynamic stress in the CVD mediation. Based on predefined inclusion and exclusion criteria, we conducted a systematic review of published scientific articles using PubMed, PMC Europe, Scopus, WoS, MEDLINE, and Google Scholar databases in the interval from 24 April 2002 to 1 April 2025. The current review included studies (n = 197) scientific articles, including new reviews, updates, and grey literature, which were evaluated according to eligibility criteria. The selection process was performed using a standardized form according to PRISMA rules, the manual search of the databases, and a double-check to ensure transparent and complete reporting of reviews. Studies had to report quantitative assessments of the relationship between vascular endothelial dysfunction, inflammation, oxidative stress, and shear stress in a chronic venous disease. Full article
(This article belongs to the Special Issue The Molecular Basis of Vascular Pathology)
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