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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pharmacology".

Deadline for manuscript submissions: closed (30 May 2023) | Viewed by 21618

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Special Issue Editor

Prof. Dr. Jeanette Woolard

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Guest Editor

Pharmacology and Neuroscience, School of Life Sciences, University of Nottingham, Nottingham NG7 2UH, UK
Interests: haemodynamics; hypertension; vascular biology; vascular endothelial growth factor (VEGF); receptor tyrosine kinase (RTK) inhibitors; cancer therapy; G-protein-coupled receptors (GPCRs); molecular pharmacology

Special Issue Information

Dear Colleagues,

The vasculature, and in particular endothelial cells, provide a major source of vasoactive substances that can produce sustained and significant effects on the cardiovascular system. Although expansive research has provided information about the physiology of the vasculature under normal and pathological conditions, we still have many unanswered questions around the mechanisms that underpin these changes, particularly in vascular disease.

Cardiovascular disease is one of the leading causes of death globally; there is a clear need to better understand the molecular pharmacology of current treatments, develop novel approaches for treating patients, and manage cardiovascular safety pharmacology over the longer term.

In this Special Issue, entitled “Molecular Pharmacology of Vascular Disease”, we aim to present research and theoretical papers addressing these issues and others related to cardiovascular disease. We invite colleagues working in this area, from structural biology and computer modelling to in vivo modelling, to submit their work for publication in this Special Issue. We believe that this Special Issue of the International Journal of Molecular Sciences will provide scientifically innovative publications, stimulating wider discussion in the field.

Prof. Dr. Jeanette Woolard
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

molecular pharmacology
vascular disease
endothelial cell function
inflammation
vascular dementia
cancer microenvironment

Published Papers (6 papers)

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Research

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17 pages, 2951 KiB

Open AccessArticle

Inhibition of p90RSK Ameliorates PDGF-BB-Mediated Phenotypic Change of Vascular Smooth Muscle Cell and Subsequent Hyperplasia of Neointima

by Ae-Rang Hwang, Hee-Jung Lee, Suji Kim, Seong-Hee Park and Chang-Hoon Woo

Int. J. Mol. Sci. 2023, 24(9), 8094; https://doi.org/10.3390/ijms24098094 - 30 Apr 2023

Cited by 2 | Viewed by 1232

Abstract

Platelet-derived growth factor type BB (PDGF-BB) regulates vascular smooth muscle cell (VSMC) migration and proliferation, which play critical roles in the development of vascular conditions. p90 ribosomal S6 kinase (p90RSK) can regulate various cellular processes through many different target substrates in several cell types, but the regulatory function of p90RSK on PDGF-BB-mediated cell migration and proliferation and subsequent vascular neointima formation has not yet been extensively examined. In this study, we investigated whether p90RSK inhibition protects VSMCs against PDGF-BB-induced cellular phenotypic changes and the molecular mechanisms underlying the effect of p90RSK inhibition on neointimal hyperplasia in vivo. Pretreatment of cultured primary rat VSMCs with FMK or BI-D1870, which are specific inhibitors of p90RSK, suppressed PDGF-BB-induced phenotypic changes, including migration, proliferation, and extracellular matrix accumulation, in VSMCs. Additionally, FMK and BI-D1870 repressed the PDGF-BB-induced upregulation of cyclin D1 and cyclin-dependent kinase-4 expression. Furthermore, p90RSK inhibition hindered the inhibitory effect of PDGF-BB on Cdk inhibitor p27 expression, indicating that p90RSK may induce VSMC proliferation by regulating the G0/G1 phase. Notably, treatment with FMK resulted in attenuation of neointima development in ligated carotid arteries in mice. The findings imply that p90RSK inhibition mitigates the phenotypic switch and neointimal hyperplasia induced by PDGF-BB. Full article

(This article belongs to the Special Issue Molecular Pharmacology of Vascular Disease)

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19 pages, 2560 KiB

Open AccessArticle

Palm Oil Derived Tocotrienol-Rich Fraction Attenuates Vascular Dementia in Type 2 Diabetic Rats

by Sohrab A. Shaikh, Rajavel Varatharajan and Arunachalam Muthuraman

Int. J. Mol. Sci. 2022, 23(21), 13531; https://doi.org/10.3390/ijms232113531 - 4 Nov 2022

Cited by 7 | Viewed by 2283

Abstract

Vascular dementia (VaD) is a serious global health issue and type 2 diabetes mellitus (T2DM) patients are at higher risk. Palm oil tocotrienol-rich fraction (TRF) exhibits neuroprotective properties; however, its effect on VaD is not reported. Hence, we evaluated TRF effectiveness in T2DM-induced VaD rats. Rats were given a single dose of streptozotocin (STZ) and nicotinamide (NA) to develop T2DM. Seven days later, diabetic rats were given TRF doses of 30, 60, and 120 mg/kg orally for 21 days. The Morris water maze (MWM) test was performed for memory assessment. Biochemical parameters such as blood glucose, plasma homocysteine (HCY) level, acetylcholinesterase (AChE) activity, reduced glutathione (GSH), superoxide dismutase (SOD) level, and histopathological changes in brain hippocampus and immunohistochemistry for platelet-derived growth factor-C (PDGF-C) expression were evaluated. VaD rats had significantly reduced memory, higher plasma HCY, increased AChE activity, and decreased GSH and SOD levels. However, treatment with TRF significantly attenuated the biochemical parameters and prevented memory loss. Moreover, histopathological changes were attenuated and there was increased PDGF-C expression in the hippocampus of VaD rats treated with TRF, indicating neuroprotective action. In conclusion, this research paves the way for future studies and benefits in understanding the potential effects of TRF in VaD rats. Full article

(This article belongs to the Special Issue Molecular Pharmacology of Vascular Disease)

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Review

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19 pages, 1457 KiB

Open AccessReview

COVID-19-Induced Myocarditis: Pathophysiological Roles of ACE2 and Toll-like Receptors

by Patrizia Pannucci, Sophie R. Jefferson, Jonathan Hampshire, Samantha L. Cooper, Stephen J. Hill and Jeanette Woolard

Int. J. Mol. Sci. 2023, 24(6), 5374; https://doi.org/10.3390/ijms24065374 - 11 Mar 2023

Cited by 8 | Viewed by 3182

Abstract

The clinical manifestations of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection responsible for coronavirus disease 2019 (COVID-19) commonly include dyspnoea and fatigue, and they primarily involve the lungs. However, extra-pulmonary organ dysfunctions, particularly affecting the cardiovascular system, have also been observed following COVID-19 infection. In this context, several cardiac complications have been reported, including hypertension, thromboembolism, arrythmia and heart failure, with myocardial injury and myocarditis being the most frequent. These secondary myocardial inflammatory responses appear to be associated with a poorer disease course and increased mortality in patients with severe COVID-19. In addition, numerous episodes of myocarditis have been reported as a complication of COVID-19 mRNA vaccinations, especially in young adult males. Changes in the cell surface expression of angiotensin-converting enzyme 2 (ACE2) and direct injury to cardiomyocytes resulting from exaggerated immune responses to COVID-19 are just some of the mechanisms that may explain the pathogenesis of COVID-19-induced myocarditis. Here, we review the pathophysiological mechanisms underlying myocarditis associated with COVID-19 infection, with a particular focus on the involvement of ACE2 and Toll-like receptors (TLRs). Full article

(This article belongs to the Special Issue Molecular Pharmacology of Vascular Disease)

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18 pages, 10098 KiB

Open AccessReview

The Endothelium and COVID-19: An Increasingly Clear Link Brief Title: Endotheliopathy in COVID-19

by Isabelle Six, Nicolas Guillaume, Valentine Jacob, Romuald Mentaverri, Said Kamel, Agnès Boullier and Michel Slama

Int. J. Mol. Sci. 2022, 23(11), 6196; https://doi.org/10.3390/ijms23116196 - 31 May 2022

Cited by 17 | Viewed by 2802

Abstract

The endothelium has a fundamental role in the cardiovascular complications of coronavirus disease 2019 (COVID-19). Infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) particularly affects endothelial cells. The virus binds to the angiotensin-converting enzyme 2 (ACE-2) receptor (present on type 2 alveolar cells, bronchial epithelial cells, and endothelial cells), and induces a cytokine storm. The cytokines tumor necrosis factor alpha, interleukin-1 beta, and interleukin-6 have particular effects on endothelial cells—leading to endothelial dysfunction, endothelial cell death, changes in tight junctions, and vascular hyperpermeability. Under normal conditions, apoptotic endothelial cells are removed into the bloodstream. During COVID-19, however, endothelial cells are detached more rapidly, and do not regenerate as effectively as usual. The loss of the endothelium on the luminal surface abolishes all of the vascular responses mediated by the endothelium and nitric oxide production in particular, which results in greater contractility. Moreover, circulating endothelial cells infected with SARS-CoV-2 act as vectors for viral dissemination by forming clusters that migrate into the circulation and reach distant organs. The cell clusters and the endothelial dysfunction might contribute to the various thromboembolic pathologies observed in COVID-19 by inducing the formation of intravascular microthrombi, as well as by triggering disseminated intravascular coagulation. Here, we review the contributions of endotheliopathy and endothelial-cell-derived extracellular vesicles to the pathogenesis of COVID-19, and discuss therapeutic strategies that target the endothelium in patients with COVID-19. Full article

(This article belongs to the Special Issue Molecular Pharmacology of Vascular Disease)

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26 pages, 19494 KiB

Open AccessReview

Novel Biomarkers of Atherosclerotic Vascular Disease—Latest Insights in the Research Field

by Cristina Andreea Adam, Delia Lidia Șalaru, Cristina Prisacariu, Dragoș Traian Marius Marcu, Radu Andy Sascău and Cristian Stătescu

Int. J. Mol. Sci. 2022, 23(9), 4998; https://doi.org/10.3390/ijms23094998 - 30 Apr 2022

Cited by 19 | Viewed by 7411

Abstract

The atherosclerotic vascular disease is a cardiovascular continuum in which the main role is attributed to atherosclerosis, from its appearance to its associated complications. The increasing prevalence of cardiovascular risk factors, population ageing, and burden on both the economy and the healthcare system have led to the development of new diagnostic and therapeutic strategies in the field. The better understanding or discovery of new pathophysiological mechanisms and molecules modulating various signaling pathways involved in atherosclerosis have led to the development of potential new biomarkers, with key role in early, subclinical diagnosis. The evolution of technological processes in medicine has shifted the attention of researchers from the profiling of classical risk factors to the identification of new biomarkers such as midregional pro-adrenomedullin, midkine, stromelysin-2, pentraxin 3, inflammasomes, or endothelial cell-derived extracellular vesicles. These molecules are seen as future therapeutic targets associated with decreased morbidity and mortality through early diagnosis of atherosclerotic lesions and future research directions. Full article

(This article belongs to the Special Issue Molecular Pharmacology of Vascular Disease)

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34 pages, 2196 KiB

Open AccessReview

Molecular Pharmacology of Inflammation Resolution in Atherosclerosis

by Stanislav Kotlyarov and Anna Kotlyarova

Int. J. Mol. Sci. 2022, 23(9), 4808; https://doi.org/10.3390/ijms23094808 - 27 Apr 2022

Cited by 14 | Viewed by 3827

Abstract

Atherosclerosis is one of the most important problems of modern medicine as it is the leading cause of hospitalizations, disability, and mortality. The key role in the development and progression of atherosclerosis is the imbalance between the activation of inflammation in the vascular wall and the mechanisms of its control. The resolution of inflammation is the most important physiological mechanism that is impaired in atherosclerosis. The resolution of inflammation has complex, not fully known mechanisms, in which lipid mediators derived from polyunsaturated fatty acids (PUFAs) play an important role. Specialized pro-resolving mediators (SPMs) represent a group of substances that carry out inflammation resolution and may play an important role in the pathogenesis of atherosclerosis. SPMs include lipoxins, resolvins, maresins, and protectins, which are formed from PUFAs and regulate many processes related to the active resolution of inflammation. Given the physiological importance of these substances, studies examining the possibility of pharmacological effects on inflammation resolution are of interest. Full article

(This article belongs to the Special Issue Molecular Pharmacology of Vascular Disease)

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