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11.4
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Cells
Special Issues
Molecular Signaling and Mechanism on Vascular Remodeling
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Molecular Signaling and Mechanism on Vascular Remodeling

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: 31 October 2026 | Viewed by 1207

Special Issue Editors

Dr. Ki Ho Park

E-Mail Website
Guest Editor
Division of Surgical Sciences, Department of Surgery, University of Virginia, Charlottesville, VA 22903, USA
Interests: vascular biology; vascular remodeling; muscle physiology; ion channels; protein therapeutics; regenerative medicine
Special Issues, Collections and Topics in MDPI journals
Dr. Yitao Huang

E-Mail Website
Guest Editor
Department of Surgery, School of Medicine, University of Virginia, Charlottesville, VA 22903, USA
Interests: vascular biology; vascular diseases; vascular remodeling; intimal hyperplasia; abdominal aortic aneurysm; epigenetic

Special Issue Information

Dear Colleagues,

Despite being among the leading global health threats, vascular diseases still suffer from a limited range of pharmacological targets and effective therapeutics, and thus require urgent attention. Vascular remodeling plays a vital role in the pathogenesis of vascular diseases, from responding to various kinds of vascular challenges to adapting to the changes in vascular homeostasis. As a result, vascular remodeling could be a potent research direction to decode the mechanism of vascular disease progression. Additionally, the cellular mechanisms of vascular remodeling, which include multiple types of vascular cells such as smooth muscle cells, endothelial cells, fibroblasts, macrophages, etc., remain poorly understood. To address this concern, this Special Issue encompasses research related to cellular mechanisms and signaling pathways during the vascular remodeling process, including atherosclerosis, aneurysm, intimal hyperplasia, and other vascular diseases. We encourage submissions covering novel targets and mechanisms underlying vascular remodeling and pathogenesis. Studies that reveal and elucidate these processes within the theme of this Special Issue will contribute to the development of pharmacological and therapeutic treatments to vascular diseases.

Dr. Ki Ho Park
Dr. Yitao Huang
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 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 diseases
  • atherosclerosis
  • aneurysm
  • intimal hyperplasia
  • vascular remodeling
  • cellular mechanisms
  • cellular signaling

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Published Papers (2 papers)

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Research

20 pages, 21622 KB  
Article
Integrin-Linked Kinase Plays an Active Role in the Regulation of Endothelial Senescence
by Wojciech M. Ciszewski, Ewa Macierzyńska-Piotrowska and Katarzyna Sobierajska
Cells 2026, 15(12), 1081; https://doi.org/10.3390/cells15121081 (registering DOI) - 14 Jun 2026
Abstract
Endothelial cells (ECs) play a critical role in physiological processes, including regulating blood fluidity, angiogenesis, and regulating the immune response. Integrins, which participate in sensing external stimuli and signal transduction, are crucial for the proper functioning of ECs. Like other cells, ECs undergo [...] Read more.
Endothelial cells (ECs) play a critical role in physiological processes, including regulating blood fluidity, angiogenesis, and regulating the immune response. Integrins, which participate in sensing external stimuli and signal transduction, are crucial for the proper functioning of ECs. Like other cells, ECs undergo senescence, which is associated with their dysfunction and contributes to increased susceptibility to cardiovascular disease. However, the role of integrin-dependent pathways in endothelial senescence is poorly understood. Here, we identify integrin-linked kinase (ILK) as a crucial factor modulating endothelial function and senescence. Using two complementary models, replicative and stress-induced premature senescence, in endothelial cells of different origins, we show that the senescent endothelium shows phenotypic and functional dysfunction. Furthermore, we revealed that these modulations correlated with ILK downregulation. Functionally, ILK depletion in young ECs was sufficient to trigger a senescence-associated phenotype and manifested key features of endothelial dysfunction. In line with this, ILK restoration in senescent cells reduced selected senescence markers and improved endothelial function. Together, these findings show that ILK is not only correlated with endothelial ageing but also works as an active regulator of senescence-linked endothelial dysfunction. Thus, ILK, as a link between adhesion-dependent signalling and endothelial ageing, is a potential target for limiting age-associated vascular decline. Full article
(This article belongs to the Special Issue Molecular Signaling and Mechanism on Vascular Remodeling)
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16 pages, 1456 KB  
Article
Cell Density-Dependent Suppression of Perlecan and Biglycan Expression by Gold Nanocluster in Vascular Endothelial Cells
by Takato Hara, Misato Saeki, Misaki Shirai, Yuichi Negishi, Chika Yamamoto and Toshiyuki Kaji
Cells 2026, 15(2), 209; https://doi.org/10.3390/cells15020209 - 22 Jan 2026
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Abstract
Proteoglycans are macromolecules consisting of a core protein and one or more glycosaminoglycan side chains. Proteoglycans synthesized by vascular endothelial cells modulate various functions such as anticoagulant activity and vascular permeability. We previously reported that some heavy metals interfere with proteoglycan expression, and [...] Read more.
Proteoglycans are macromolecules consisting of a core protein and one or more glycosaminoglycan side chains. Proteoglycans synthesized by vascular endothelial cells modulate various functions such as anticoagulant activity and vascular permeability. We previously reported that some heavy metals interfere with proteoglycan expression, and that organic–inorganic hybrid molecules, such as metal complexes and organometallic compounds, serve as useful tools to analyze proteoglycan synthesis mechanisms. However, the effects of metal compounds lacking electrophilicity on proteoglycan synthesis remain unclear. Au25(SG)18, a nanoscale gold cluster consisting of a metal core protected by gold–glutathione complexes, exhibits extremely low intramolecular polarity. In this study, we investigated the effect of Au25(SG)18 on proteoglycan synthesis in vascular endothelial cells. Au25(SG)18 accumulated significantly in vascular endothelial cells at low cell density and suppressed the expression of perlecan, a major heparan sulfate proteoglycan in cells, by inactivating ADP-ribosylation factor 6 (Arf6). Additionally, Au25(SG)18 reduced the expression of biglycan, a small dermatan sulfate proteoglycan, in vascular endothelial cells at low cell density; however, the underlying mechanisms remain unclear. Overall, our findings suggest that organic–inorganic hybrid molecules regulate the activity of Arf6-mediated protein transport to the extracellular space and that perlecan is regulated through this mechanism, highlighting the importance of Arf6-mediated extracellular transport for maintaining vascular homeostasis. Full article
(This article belongs to the Special Issue Molecular Signaling and Mechanism on Vascular Remodeling)
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