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Vascular Biology in Health and Diseases

A Special Issue of Current Issues in Molecular Biology (ISSN 1467-3045) belonging to the section "Biochemistry, Molecular and Cellular Biology".

Deadline for manuscript submissions: 31 December 2026 | Viewed by 3942

Editor

Prof. Dr. Nilanjana Maulik

E-Mail Website
Guest Editor
Molecular Cardiology and Angiogenesis Laboratory, Department of Surgery, University of Connecticut School of Medicine, UConn Health, 263 Farmington Avenue, Farmington, CT 06030, USA
Interests: therapeutic angiogenesis; ischemic heart; signal transduction; tissue repair and regeneration; gene expression; apoptosis; diabetic cardiomyopathy; exosome; peripheral artery disease; sepsis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Vascular biology is important for understanding how blood vessels and cell regeneration are affected by various disease conditions. Vascular disease is a balance between vascular injury and vascular repair. Blood vessels are constantly exposed to various responses and insults. As we know, hypertension is not a disease, but it is a marker for vascular dysfunction. Endothelial and vascular smooth muscle dysfunction precedes the development of various vascular diseases. The endothelium maintains the main vascular health. Therefore, it is essential to investigate the molecular and physiological conditions related to angiogenesis and cellular architecture within vascular tissues. In addition, vascular Biology plays an important role in the initiation of hypertension, cardiovascular disease (CVD), and target organ damage (TOD). Oxidative stress, inflammation, and immunological reactions initiate various pathological pathways to induce CVD and TOD. Various vitamins, antioxidants, minerals, and drugs can prevent these disease conditions through numerous vascular biology mechanisms. Therefore, it is always beneficial to connect basic molecular research with clinical applications, encompassing vascular disease biomarkers, new therapeutics, precision medicine, and preclinical tools.

Prof. Dr. Nilanjana Maulik
Guest Editor

Manuscript Submission Information

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Keywords

  • vascular biology
  • vascular disease
  • endothelium
  • cardiovascular disease (CVD)
  • pathological mechanisms

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Published Papers (4 papers)

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Research

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18 pages, 5354 KB  
Article
The Bath Additive KTPB Induces an Angiogenesis-Associated Transcriptional Program Without Detectable Cytotoxicity in Human Vascular Endothelial Cells
by Norihiro Otani, Kieu D. M. Nguyen, Kiyoshi Maehara, Jiawei Wan, Atsushi Hirokawa and Takehito Sugasawa
Curr. Issues Mol. Biol. 2026, 48(9), 895; https://doi.org/10.3390/cimb48090895 - 1 Sep 2026
Viewed by 223
Abstract
Regular bathing is a common habit worldwide, yet bath additives have been characterized almost exclusively at the physiological level, while their molecular effects on human cells remain largely unexplored. We previously showed by RNA sequencing (RNA-seq) that the complex bath additive Karada Totonou [...] Read more.
Regular bathing is a common habit worldwide, yet bath additives have been characterized almost exclusively at the physiological level, while their molecular effects on human cells remain largely unexplored. We previously showed by RNA sequencing (RNA-seq) that the complex bath additive Karada Totonou ProBath (KTPB) induced the expression of EGR1 and hyaluronic acid synthase genes in human keratinocytes and fibroblasts, which represent the vascular endothelial growth factor (VEGF)-producing side of the cutaneous angiogenic axis; whether the VEGF-receiving endothelium responds to KTPB was unknown. Here, human vascular endothelial cells were exposed to KTPB and profiled by RNA-seq, and cytotoxicity was assessed using resazurin and Hoechst assays. KTPB altered gene expression in a time-dependent manner, and the differentially expressed genes were classified into three clusters with distinct temporal profiles: a late-repressed cluster, a transiently induced cell cycle-associated cluster, and a late-induced cluster enriched for blood vessel development and VEGFA-VEGFR2 signaling. The angiogenesis-related genes ID1, ID3, and EDN1 were markedly upregulated, peaking at 1–2 h. KTPB showed no detectable cytotoxicity in this cell model at any of the tested concentrations, which spanned the recommended use range. These results indicate that KTPB elicits an angiogenesis-associated transcriptional program in vascular endothelial cells without compromising viability and highlight transcriptomics’ value for characterizing bath additives. Full article
(This article belongs to the Special Issue Vascular Biology in Health and Diseases)
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20 pages, 6343 KB  
Article
Protective Effect of Apocynum venetum L. Leaves Extract Against Diabetic Cardiomyopathy: Inhibition of Oxidative Stress and Ferroptosis via Modulation of the Xc−/GSH/GPX4 Axis
by Subinuer Abuduaini, Guohua Shi, Li Chen, Subinuer Erreken, Mei Long, Xiaoqian Tang and Jinsen Kang
Curr. Issues Mol. Biol. 2026, 48(4), 375; https://doi.org/10.3390/cimb48040375 - 3 Apr 2026
Viewed by 938
Abstract
Background: Diabetic cardiomyopathy (DCM), a common cardiovascular complication associated with diabetes mellitus, has the potential to progress to heart failure. Apocynum venetum L. leaves extract (AVLE) possesses known cardioprotective activity, but its effect on DCM remains unclear. This study explored the protective effects [...] Read more.
Background: Diabetic cardiomyopathy (DCM), a common cardiovascular complication associated with diabetes mellitus, has the potential to progress to heart failure. Apocynum venetum L. leaves extract (AVLE) possesses known cardioprotective activity, but its effect on DCM remains unclear. This study explored the protective effects of AVLE against myocardial injury in type 2 diabetes and the underlying mechanisms. Methods: DCM was established in vivo using db/db mice and in vitro using high-glucose, high-fat (HGHF)-stimulated H9c2 cardiomyocytes. We evaluated metabolic profiles, cardiac function, histopathology, oxidative stress, inflammation, and ferroptosis. Results: In vivo, following 12 weeks of AVLE treatment, cardiac function and structural integrity were significantly improved, serum cardiac injury markers and dyslipidemia were reduced, and pathological myocardial remodeling was attenuated in db/db mice; in vitro, AVLE enhanced cell viability and attenuated cellular damage under HGHF conditions. Mechanistically, AVLE alleviated oxidative stress and inflammation, restored mitochondrial function, and inhibited ferroptosis by regulating key pathway proteins; it upregulated GPX4 and SLC7A11, while downregulating TfR1 and ACSL4. Conclusions: AVLE exerts cardioprotective effects against diabetic cardiomyopathy by reducing oxidative stress and inflammation, mitigating lipid peroxidation and mitochondrial damage, ultimately inhibiting ferroptosis through regulation of the Xc−/GSH/GPX4 axis. Full article
(This article belongs to the Special Issue Vascular Biology in Health and Diseases)
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15 pages, 3837 KB  
Article
Extracellular Adenosine Contributes to the Hydrogen Peroxide-Induced Calcification of Cultured Tendon Cells
by Tomomi Sakuma, Chantida P. N. Mahasarakham, Xin Lin, Hiroyuki Yoshitake, Akira Nifuji, Masaki Noda and Yoichi Ezura
Curr. Issues Mol. Biol. 2026, 48(3), 244; https://doi.org/10.3390/cimb48030244 - 26 Feb 2026
Viewed by 1320
Abstract
Background: Well-known risk factors for soft tissue heterotopic ossification (HO) include aging and mechanical stress, which may be linked to oxidative stress and downstream nucleotide metabolites. Thus, we investigated the involvement of extracellular ATP (ex-ATP) and its metabolites in the oxidative stress-induced mineralization [...] Read more.
Background: Well-known risk factors for soft tissue heterotopic ossification (HO) include aging and mechanical stress, which may be linked to oxidative stress and downstream nucleotide metabolites. Thus, we investigated the involvement of extracellular ATP (ex-ATP) and its metabolites in the oxidative stress-induced mineralization of TT-D6 cells and primary mouse tendon cells. Methods: An osteogenic culture with the intermittent addition of hydrogen peroxide was monitored for two weeks using metabolomic and gene expression analyses. Results: Calcium deposition was significantly enhanced by 0.3 mM hydrogen peroxide in the osteogenic media after 2 weeks, with minimal calcification in its absence. Similar results were observed in a medium transfer experiment using 3-day-old hydrogen peroxide-treated conditioned medium, which led to an increased expression of osterix and alkaline phosphatase. Metabolomic analysis revealed a gradual increase in ex-ATP and its metabolites, including ADP, AMP, and adenosine, in the medium. The metabolite increase was enhanced by hydrogen peroxide after 12 h. Moreover, exogenous adenosine (100 μM) increased mineralization in osteogenic media. Additionally, 1 μM dipyridamole, an inhibitor of equilibrative nucleoside transporter 1 (Ent1), also increased it in response to low-dose (0.1 mM) hydrogen peroxide. Conclusions: The enhanced osteogenic calcification of the tendon cell culture by hydrogen peroxide was associated with an increase in extracellular nucleotide metabolites, especially adenosine, with some evidence of causality. Full article
(This article belongs to the Special Issue Vascular Biology in Health and Diseases)
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Review

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27 pages, 8280 KB  
Review
Gla-Rich Protein (GRP): A Vitamin K-Dependent Regulator of Vascular Calcification, Inflammation, and Mineral Homeostasis
by Antun Loncaric and Lara Baticic
Curr. Issues Mol. Biol. 2026, 48(5), 458; https://doi.org/10.3390/cimb48050458 - 29 Apr 2026
Viewed by 941
Abstract
Gla-rich protein (GRP), also known as UCMA, is a vitamin K-dependent protein that has emerged as an important regulator of pathological calcification and inflammation. Vascular calcification is a major complication of chronic kidney disease and cardiovascular disorders and is now recognized as an [...] Read more.
Gla-rich protein (GRP), also known as UCMA, is a vitamin K-dependent protein that has emerged as an important regulator of pathological calcification and inflammation. Vascular calcification is a major complication of chronic kidney disease and cardiovascular disorders and is now recognized as an active and tightly regulated process rather than a passive accumulation of minerals. Increasing evidence indicates that GRP plays a protective role in mineral homeostasis through its strong calcium-binding capacity and its dependence on vitamin K-mediated gamma carboxylation. This work represents a comprehensive narrative review aimed at summarizing and critically discussing the current scientific knowledge on GRP. Available experimental and clinical data are analyzed with respect to gene expression, molecular regulation, vitamin K dependency, and underlying mechanisms of action. Particular emphasis is placed on the dual function of GRP in inhibiting ectopic calcification and modulating inflammatory responses. The evidence linking altered GRP levels or changes in its carboxylation status with chronic kidney disease, vascular calcification, calcific aortic valve disease, osteoarthritis, and tumor-associated microcalcifications is systematically examined. Current findings collectively support the concept that GRP is a multifunctional protein operating at the interface of mineral metabolism, inflammation, and tissue remodeling. Despite promising experimental data, important knowledge gaps remain, including the absence of standardized assays capable of distinguishing different GRP forms and the lack of longitudinal clinical studies evaluating its predictive value. This manuscript highlights the potential of GRP as a biomarker of disturbed mineral homeostasis and cardiovascular risk, while emphasizing the need for further research to clarify its precise biological functions and clinical relevance. Full article
(This article belongs to the Special Issue Vascular Biology in Health and Diseases)
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