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Molecular Insights into Atherosclerosis and Vascular Endothelial Cells
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Molecular Insights into Atherosclerosis and Vascular Endothelial Cells

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 May 2025 | Viewed by 6864

Special Issue Editor

Prof. Dr. Yasuyuki Fujiwara

E-Mail Website
Guest Editor
Department of Environmental Health, School of Pharmacy, Tokyo University of Pharmacy and Life Sciences, Hachioji 192-0392, Japan
Interests: reactive oxygen species; oxidative stress; shear stress; inflammation; adhesion molecule; vascular permeability; vascular morphology; vascular toxicity; apoptosis; vascular disease; atherosclerosis; proliferation; migration; metallothionein
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Atherosclerosis is a major cause of many cardiovascular diseases, and its etiology and mechanisms are rather complex. However, as evident from previous research, dysfunction of vascular endothelial cells is generally recognized as the starting point.

In this Special Issue, we welcome submissions of recent reviews, original papers, short communications, as well as perspectives that provide a clarification of the underlying mechanisms determining the onset, progression, and complications of atherosclerosis, thereby leading to the development of future therapeutic approaches and preventive strategies.

Potential topics related to vascular endothelial cell research include the following:

  • Inflammatory responses;
  • Oxidative stress;
  • Mechanical and rheological stress;
  • Regulation of blood coagulation-fibrinolysis system;
  • Cell–cell interactions;
  • Cell–extracellular matrix interactions;
  • Novel risk factors and other significant contributors

Dr. Takato Hara (from Toho University, Japan) is a good scientist serving as the Topical Advisory Panel in IJMS, who will assist Prof. Fujiwara in managing this Special Issue.

Prof. Dr. Yasuyuki Fujiwara
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.

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Published Papers (5 papers)

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Research

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15 pages, 1700 KiB  
Article
Reduced Oxidative Susceptibility of Lp(a) and LDL Fractions as a Pleiotropic Effect of Lipoprotein Apheresis in Patients with Elevated Lp(a) and ASCVDs
by Aleksandra Krzesińska, Joanna Marlęga-Linert, Gabriela Chyła-Danił, Marta Marcinkowska, Paulina Rogowska, Katarzyna Stumska, Marcin Fijałkowski, Marcin Gruchała, Maciej Jankowski, Agnieszka Mickiewicz and Agnieszka Kuchta
Int. J. Mol. Sci. 2024, 25(24), 13597; https://doi.org/10.3390/ijms252413597 - 19 Dec 2024
Abstract
Oxidative modifications of lipoproteins play a crucial role in the initiation of atherosclerotic cardiovascular diseases (ASCVDs). Nowadays, the one effective strategy for the treatment of patients with hyperlipoproteinemia(a) is lipoprotein apheresis (LA), which has a pleiotropic effect on reducing the risk of ASCVDs. [...] Read more.
Oxidative modifications of lipoproteins play a crucial role in the initiation of atherosclerotic cardiovascular diseases (ASCVDs). Nowadays, the one effective strategy for the treatment of patients with hyperlipoproteinemia(a) is lipoprotein apheresis (LA), which has a pleiotropic effect on reducing the risk of ASCVDs. The significance of oxidative susceptibility of the LDL fraction in ASCVDs has been extensively studied. Whether LA alters the susceptibility of lipoprotein(a) to oxidative modifications remains an unresolved issue. In this study, we isolated lipoprotein fractions by ultracentrifugation in patients with hyperlipoproteinemia(a) undergoing apheresis (LA group) at three time points and patients who were qualified for LA but did not consent to the procedure (non-LA group). We performed copper-mediated oxidation of Lp(a) and LDL fractions and determined autotaxin activity. After apheresis, we observed a lower susceptibility to oxidation of the Lp(a) and LDL fractions as expressed by the extended value of oxidation lag time, decreased slope of the oxidation curve, and decreased final concentration of conjugated dienes. No significant differences were found between these parameters before and 7 days after LA. Additionally, both patients undergoing and not undergoing LA had a significant correlation between autotaxin activity and all parameters characterizing susceptibility to oxidation in the Lp(a) fraction. Our results demonstrate that the pleiotropic effect of apheresis may be related to the reduced oxidative susceptibility of Lp(a) and LDL particles, which may influence the reduction in ASCVD risk in patients undergoing apheresis. The results of the rebound effect 7 days after LA will contribute to a better definition of apheresis frequency guidelines. Full article
(This article belongs to the Special Issue Molecular Insights into Atherosclerosis and Vascular Endothelial Cells)
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13 pages, 2158 KiB  
Article
Ticagrelor Induces Angiogenesis in Progenitor and Mature Endothelial Cells In Vitro: Investigation of the Possible Role of Adenosine
by Sofia Sidiropoulou, Aikaterini Gatsiou, Kenny M. Hansson, Aikaterini N. Tsouka, Konstantinos Stellos and Alexandros D. Tselepis
Int. J. Mol. Sci. 2024, 25(24), 13343; https://doi.org/10.3390/ijms252413343 - 12 Dec 2024
Viewed by 764
Abstract
Ticagrelor, a reversible platelet P2Y12 receptor antagonist, exerts various pleiotropic actions, some of which are at least partially mediated through adenosine. We studied the ticagrelor and adenosine effect on the angiogenic properties of progenitor CD34+-derived endothelial colony-forming cells (ECFCs). Angiogenesis [...] Read more.
Ticagrelor, a reversible platelet P2Y12 receptor antagonist, exerts various pleiotropic actions, some of which are at least partially mediated through adenosine. We studied the ticagrelor and adenosine effect on the angiogenic properties of progenitor CD34+-derived endothelial colony-forming cells (ECFCs). Angiogenesis studies were performed in vitro using capillary-like tube formation and spheroid-based angiogenesis assays. The effects of adenosine receptor antagonists, including DPCPX (A1 antagonist), SCH58621 (A2A antagonist), MRS1706 (A2B inverse agonist and antagonist), MRS1220 (A3 antagonist) and adenosine deaminase (ADA), were also investigated. Ticagrelor, adenosine, and their combination increased capillary-like tube formation and spheroid sprout formation by ECFCs in a dose-dependent manner. This effect was significantly reduced by SCH58621, MRS1706, and their combination, as well as by ADA. By contrast, DPCPX and MRS1220 did not exhibit any inhibitory effects. Similar results were obtained when mature human umbilical vein endothelial cells (HUVECs) were studied. These results show that ticagrelor stimulates angiogenesis by progenitor and mature endothelial cells in an adenosine-dependent pathway in which the adenosine receptors A2A and A2B play major roles. The significance of these results at the clinical level in patients with atherothrombotic events and treated with ticagrelor needs to be investigated. Full article
(This article belongs to the Special Issue Molecular Insights into Atherosclerosis and Vascular Endothelial Cells)
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13 pages, 2764 KiB  
Article
Cadmium Induces Vascular Endothelial Cell Detachment by Downregulating Claudin-5 and ZO-1 Levels
by Takato Hara, Mayuka Asatsu, Tatsuya Yamagishi, Chinami Ohata, Hitomi Funatsu, Yuzuki Takahashi, Misaki Shirai, Chiaki Nakata, Haruka Katayama, Toshiyuki Kaji, Tomoya Fujie and Chika Yamamoto
Int. J. Mol. Sci. 2024, 25(20), 11035; https://doi.org/10.3390/ijms252011035 - 14 Oct 2024
Viewed by 890
Abstract
Cadmium is a contributing factor to cardiovascular diseases and highly toxic to vascular endothelial cells. It has a distinct mode of injury, causing the de-endothelialization of regions in the monolayer structure of endothelial cells in a concentration-dependent manner. However, the specific molecules involved [...] Read more.
Cadmium is a contributing factor to cardiovascular diseases and highly toxic to vascular endothelial cells. It has a distinct mode of injury, causing the de-endothelialization of regions in the monolayer structure of endothelial cells in a concentration-dependent manner. However, the specific molecules involved in the cadmium toxicity of endothelial cells remain unclear. The purpose of this study was to identify the specific molecular mechanisms through which cadmium affects endothelial detachment. Cadmium inhibited the expression of claudin-5 and zonula occludens (ZO)-1, which are components of tight junctions (strongest contributors to intercellular adhesion), in a concentration- and time-dependent manner. Compared to arsenite, zinc, and manganese, only cadmium suppressed the expression of both claudin-5 and ZO-1 molecules. Moreover, the knockdown of claudin-5 and ZO-1 exacerbated cadmium-induced endothelial cell injury and expansion of the detachment area, whereas their overexpression reversed these effects. CRE-binding protein inhibition reduced cadmium toxicity, suggesting that CRE-binding protein activation is involved in the cadmium-induced inhibition of claudin-5 and ZO-1 expression and endothelial detachment. These findings provide new insights into the toxicological mechanisms of cadmium-induced endothelial injury and risk of cardiovascular disease. Full article
(This article belongs to the Special Issue Molecular Insights into Atherosclerosis and Vascular Endothelial Cells)
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8 pages, 514 KiB  
Communication
A Potential Link between Myeloperoxidase Modified LDL, Atherosclerosis and Depression
by Jalil Daher
Int. J. Mol. Sci. 2024, 25(16), 8805; https://doi.org/10.3390/ijms25168805 - 13 Aug 2024
Viewed by 1159
Abstract
Atherosclerosis is a chronic inflammatory disease that involves modified low-density lipoproteins (LDL) which play a pivotal role in the initiation and progression of the disease. Myeloperoxidase oxidized LDL (Mox-LDL) is considered to be the most patho-physiologically relevant type of modified LDL and has [...] Read more.
Atherosclerosis is a chronic inflammatory disease that involves modified low-density lipoproteins (LDL) which play a pivotal role in the initiation and progression of the disease. Myeloperoxidase oxidized LDL (Mox-LDL) is considered to be the most patho-physiologically relevant type of modified LDL and has been reported to be ubiquitously present in atheroma plaques of patients with atherosclerosis. Besides its involvement in the latter disease state, Mox-LDL has also been shown to be implicated in the pathogenesis of various illnesses including sleep disorders, which are in turn associated with heart disease and depression in many intricate ways. Meanwhile, we have recently shown that lox-1-mediated Mox-LDL signaling modulates neuroserpin activity in endothelial cells, which could have major implications that go beyond the pathophysiology of stroke and cerebrovascular disease (CD). Of note is that tissue plasminogen activator (tPA), which is the main target of neuroserpin in the brain, has a crucial function in the processing of brain-derived neurotrophic factor (BDNF) into its mature form. This factor is known to be involved in major depressive disorder (MDD) development and pathogenesis. Since tPA is more conventionally recognized as being involved in fibrinolytic mechanisms, and its effect on the BDNF system in the context of MDD is still not extensively studied, we speculate that any Mox-LDL-driven change in the activity of tPA in patients with atherosclerosis may lead to a decrease in the production of mature BDNF, resulting in impaired neural plasticity and depression. Deciphering the mechanisms of interaction between those factors could help in better understanding the potentially overlapping pathological mechanisms that regulate disease processes in CD and MDD, supporting the possibility of novel and common therapeutic opportunities for millions of patients worldwide. Full article
(This article belongs to the Special Issue Molecular Insights into Atherosclerosis and Vascular Endothelial Cells)
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Review

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16 pages, 2250 KiB  
Review
Molecular Mechanisms Regulating Vascular Endothelial Permeability
by Rio Wakasugi, Kenji Suzuki and Takako Kaneko-Kawano
Int. J. Mol. Sci. 2024, 25(12), 6415; https://doi.org/10.3390/ijms25126415 - 11 Jun 2024
Cited by 1 | Viewed by 2804
Abstract
Vascular endothelial cells form a monolayer in the vascular lumen and act as a selective barrier to control the permeability between blood and tissues. To maintain homeostasis, the endothelial barrier function must be strictly integrated. During acute inflammation, vascular permeability temporarily increases, allowing [...] Read more.
Vascular endothelial cells form a monolayer in the vascular lumen and act as a selective barrier to control the permeability between blood and tissues. To maintain homeostasis, the endothelial barrier function must be strictly integrated. During acute inflammation, vascular permeability temporarily increases, allowing intravascular fluid, cells, and other components to permeate tissues. Moreover, it has been suggested that the dysregulation of endothelial cell permeability may cause several diseases, including edema, cancer, and atherosclerosis. Here, we reviewed the molecular mechanisms by which endothelial cells regulate the barrier function and physiological permeability. Full article
(This article belongs to the Special Issue Molecular Insights into Atherosclerosis and Vascular Endothelial Cells)
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