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Cells
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Molecular Insights into Vascular Physiology and Pathology
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Molecular Insights into Vascular Physiology and Pathology

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: 31 March 2026 | Viewed by 2092

Special Issue Editor

Dr. Suravi Majumder

E-Mail Website
Guest Editor
Department of Internal Medicine, McGovern Medical School, University of Texas Health Science Center, Houston, TX, USA
Interests: vascular disease; cell signaling; cell biology

Special Issue Information

Dear Colleagues,

We are pleased to invite you to contribute to our Special Issue on "Molecular Insights into Vascular Physiology and Pathology". Vascular health is a cornerstone of overall well-being, and advances in understanding the molecular mechanisms underlying vascular function and dysfunction have led to significant improvements in the prevention, diagnosis, and treatment of cardiovascular diseases. This Special Issue aims to bring together leading researchers and scientists to share their latest findings and insights on the complex molecular processes that regulate vascular physiology and contribute to vascular pathology.

The vascular system is a dynamic network of blood vessels that transports oxygen, nutrients, and waste products throughout the body. It plays a critical role in maintaining tissue homeostasis and responding to various stimuli, including hormones, neurotransmitters, and mechanical forces. In recent years, significant progress has been made in elucidating the molecular mechanisms that regulate vascular tone, angiogenesis, inflammation, and thrombosis.  However, many questions remain regarding the intricate interplay between multiple factors that contribute to vascular disease and the development of novel therapeutic approaches for vascular diseases.

In this Special Issue, original research articles and comprehensive reviews are welcome. Research areas may include (but not limited to) the following:

  • The role of endothelial cells in vascular homeostasis and disease;
  • The role of vascular smooth muscle cells in the progression of vascular diseases;
  • Molecular mechanism of vascular remodeling ;
  • Vascular signaling;
  • Vascular aging;
  • Genetic and epigenetic factors influencing vascular function and disease progression;
  • Vascular inflammation and immune responses in atherosclerosis and aneurysm formation;
  • Advances in imaging techniques and biomarker discovery for assessing vascular health;
  • Novel therapeutic approaches for treating cardiovascular diseases;
  • Role of Artificial Intelligence and machine learning approaches in diagnosing and treating vascular disease.

We encourage contributions from a wide range of disciplines, including cell biology, molecular biology, genetics, immunology, physiology, and pathology. By sharing our collective knowledge and expertise, we can continue to advance the field of vascular biology and improve patient outcomes.

We look forward to receiving your contributions.

Dr. Suravi Majumder
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 250 words) can be sent to the Editorial Office for assessment.

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. Cells is an international peer-reviewed open access semimonthly 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 2700 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 physiology
  • vascular pathology
  • endothelial cells
  • vascular smooth muscle cells
  • vascular inflammation
  • vascular signaling
  • vascular aging
  • vascular remodeling
  • atherosclerosis
  • cardiovascular diseases
  • biomarkers
  • novel therapeutic approaches

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  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
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  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • Reprint: MDPI Books provides the opportunity to republish successful Special Issues in book format, both online and in print.

Further information on MDPI's Special Issue policies can be found here.

Published Papers (3 papers)

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Research

19 pages, 4352 KB  
Article
Human Pericardial Fluid-Derived Cells Exhibit Mesothelial-like Properties and Exert Proangiogenic Effects on Endothelial Cells
by Konstantin Dergilev, Alexander Zubko, Irina Beloglazova, Zoya Tsokolaeva, Ekaterina Azimova, Aleria Dolgodvorova, Irina Iarushkina, Alexander Andreev, Andrey Shiryaev, Pavel Docshin, Anna Malashicheva and Yelena Parfyonova
Cells 2025, 14(23), 1855; https://doi.org/10.3390/cells14231855 - 25 Nov 2025
Viewed by 226
Abstract
Modern therapies aimed at stimulating heart vascularization are critical for regenerating damaged heart tissue and treating ischemic heart disease. Approaches based on developmental biology concepts, particularly those involving the use of cells to coordinate vascular network formation, are of great interest. In this [...] Read more.
Modern therapies aimed at stimulating heart vascularization are critical for regenerating damaged heart tissue and treating ischemic heart disease. Approaches based on developmental biology concepts, particularly those involving the use of cells to coordinate vascular network formation, are of great interest. In this context, epicardial mesothelial cells (MCs) have emerged as a key regulator of blood and lymphatic vessel development during cardiogenesis. However, therapeutic targeting of MCs remains challenging because of anatomical constraints and the difficulties related to isolation of viable cell cultures for research. In this study, we demonstrate for the first time that the pericardial fluid contains cell layers, being an easily accessible source of cardiac MCs. These cells exhibit a characteristic epithelial-like morphology and robust in vitro proliferation, and an ability to undergo epicardial-to-mesenchymal transition in response to TGFβ1. They secrete a broad range of proangiogenic and proinflammatory factors and exert a potent effect on endothelial cells, stimulating proangiogenic behavior and promoting vascular structure formation on MatrigelTM. Treating MCs with TGF-β1 enhances the secretion of VEGF, G-CSF, GM-CSF and MCP-3, thereby boosting their proangiogenic properties. Therefore, pericardial fluid is an easily accessible source of MCs for studying their regulatory mechanisms, for being applied in tissue engineering, and for developing approaches to improve heart vascularization. Full article
(This article belongs to the Special Issue Molecular Insights into Vascular Physiology and Pathology)
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18 pages, 3066 KB  
Article
Opioid System Antagonism Alters Vascular Proteome and Collagen Deposition in ApoE−/− Mice
by Kinga Jaskuła, Agata Nawrocka, Piotr Poznański, Aneta Stachowicz, Marzena Łazarczyk, Mariusz Sacharczuk and Dominik S. Skiba
Cells 2025, 14(19), 1559; https://doi.org/10.3390/cells14191559 - 8 Oct 2025
Viewed by 766
Abstract
Atherosclerosis is common cardiovascular disease, leading to complications such as myocardial infarction and stroke. The main causes of these diseases are lipid accumulation and inflammation in large arteries. In this study, we investigated whether opioid receptor blockade impacts factors involved in atherosclerosis development. [...] Read more.
Atherosclerosis is common cardiovascular disease, leading to complications such as myocardial infarction and stroke. The main causes of these diseases are lipid accumulation and inflammation in large arteries. In this study, we investigated whether opioid receptor blockade impacts factors involved in atherosclerosis development. We administered naloxone to 8-week-old and 36-week-old ApoE−/− mice, then examined the expression of Col1a1, and Col3a1 in the aorta, as well as the influence of naloxone administration on aortic collagen layer thickness and proteomic changes in the aorta. Additionally, we assessed the impact of naloxone on the splenic T-cell populations. The results showed that Col3a1 expression decreased in young mice but increased in older mice. In 36-week-old mice, naloxone administration led to an increase in aortic collagen layer thickness, but remained unchanged in young mice. Proteomic analysis identified 587 proteins that were altered following naloxone treatment. Our studies suggest that the opioid system is an important factor in atherosclerosis development. Full article
(This article belongs to the Special Issue Molecular Insights into Vascular Physiology and Pathology)
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Graphical abstract

13 pages, 12268 KB  
Article
Inflammation in Cerebral Cavernous Malformations: Differences Between Malformation Related Epilepsy vs. Symptomatic Hemorrhage
by Jan Rodemerk, Adrian Engel, Julius L. H. Horstmann, Laurèl Rauschenbach, Marvin Darkwah Oppong, Alejandro N. Santos, Andreas Junker, Cornelius Deuschl, Michael Forsting, Yuan Zhu, Ramazan Jabbarli, Karsten H. Wrede, Börge Schmidt, Ulrich Sure and Philipp Dammann
Cells 2025, 14(19), 1510; https://doi.org/10.3390/cells14191510 - 27 Sep 2025
Viewed by 762
Abstract
Background and Objective: Cerebral cavernous malformation (CCM) is a vascular disorder causing seizures, neurological deficits, and hemorrhagic stroke. It can be sporadic or inherited via CCM1, CCM2, or CCM3 gene mutations. Inflammation is broadly recognized as a promoter of cerebral vascular malformations. This [...] Read more.
Background and Objective: Cerebral cavernous malformation (CCM) is a vascular disorder causing seizures, neurological deficits, and hemorrhagic stroke. It can be sporadic or inherited via CCM1, CCM2, or CCM3 gene mutations. Inflammation is broadly recognized as a promoter of cerebral vascular malformations. This study explores inflammatory mechanisms and differences behind CCM-related hemorrhage and epilepsy. Material and Methods: The study group comprised 28 patients, ten patients with CCM-related epilepsy, and 18 patients who clinically presented with a cerebral hemorrhage at diagnosis. All patients underwent microsurgical resection of the CCMs. Formaldehyde-fixed, paraffin-embedded tissue samples were immunohistochemically stained using a monoclonal antibody against Cyclooxygenase 2 (COX-2) (Dako, Santa Clara, CA; Clone: CX-294) and NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) (ABCAM, Cambridge, MA, USA; ab214185). MRI and clinical data were correlated with immunohistochemical findings, and the analysis was conducted utilizing the Trainable Weka Segmentation algorithm. Results: Median CCM volume was 1.68 cm3 (IQR: 0.85–3.07 cm3). There were significantly more NLRP3-positive cells (32.56% to 91.98%; mean: 65.82%, median: 68.34%; SD: ±17.70%), compared to COX-2-positive cells (1.82% to 79.69%; mean: 45.87%, median: 49.06%; SD: ±22.56%). No correlation was shown between the volume of CCMs and a hemorrhage event (p = 0.13, 95% CI: 0.99–1.02). Symptomatic brain hemorrhage showed a significantly increased inflammatory enzyme upregulation from both COX-2 (p < 0.001) and NLRP3 (p = 0.009) versus patients with symptomatic CCM-related epilepsy at first diagnosis. Conclusions: Inflammatory processes in CCMs seem to be driven by broad and multiple pathways because both COX-2 and NLRP3-driven inflammatory pathways are consistently activated. As a novelty, this study showed that patients with symptomatic hemorrhage showed upregulated inflammatory enzyme activity compared to patients with CCM-related epilepsy. No direct links between NLRP3, COX-2 expression, and radiological, pathological, or preexisting patient conditions were found. Full article
(This article belongs to the Special Issue Molecular Insights into Vascular Physiology and Pathology)
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