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Endothelial Dysfunction: Pathophysiology and Molecular Mechanisms 2.0
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Endothelial Dysfunction: Pathophysiology and Molecular Mechanisms 2.0

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: closed (31 December 2020) | Viewed by 12129

Special Issue Editors

Prof. Dr. Francesco Perticone

E-Mail Website
Guest Editor
Department of Medical and Surgical Sciences, University Magna Græcia, 88100 Catanzaro, Italy
Interests: endothelial dysfunction; arterial stiffness; hypertension; atherosclerosis; metabolic syndrome; diabetes mellitus; cardiovascular risk; insulin resistance
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Maria Perticone

E-Mail Website
Guest Editor
Department of Medical and Surgical Sciences, University Magna Græcia, 88100 Catanzaro, Italy
Interests: obesity; type-2 diabetes; metabolic syndrome; endothelial dysfunction; hypertension; target organ damage
Special Issues, Collections and Topics in MDPI journals
Dr. Raffaele Maio

E-Mail Website
Guest Editor
Geriatrics Unit, Azienda Ospedaliero Universitaria “Mater Domini”, 88100 Catanzaro, Italy
Interests: hypertension; endothelial dysfunction; ischemic heart disease; arrhythmia; target organ damage; cardiovascular risk factors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Endothelial dysfunction is an early step of the atherosclerotic process. It is well established that the initiation and progression of disease, and its later activation to increase the risk of morbid events, depends on profound dynamic changes in vascular biology. The endothelium is emerged as the key regulator of vascular homeostasis, in that it has not merely a barrier function but also acts as an active signal transducer for circulating influences that modify the vessel wall phenotype. Alteration in endothelial function precedes the development of morphological atherosclerotic changes and can also contribute to lesion development and later clinical complications. Furthermore, in the last few decades, the relationship between vascular and metabolic diseases has been deeply investigated, demonstrating a close link between endothelial dysfunction and insulin resistance.

This Special Issue “Endothelial Dysfunction: Pathophysiology and Molecular Mechanisms 2.0” will cover a selection of recent research topics and current review articles in the field of endothelial activation in cardio-metabolic diseases.

Prof. Dr. Francesco Perticone
Dr. Maria Perticone
Dr. Raffaele Maio
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 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

  • endothelial dysfunction
  • nitric oxide
  • atherosclerosis
  • arterial stiffness
  • vascular aging
  • cardiovascular risk
  • insulin resistance

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Published Papers (2 papers)

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Research

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16 pages, 1959 KiB  
Article
Glucose-6-Phosphate Dehydrogenase Deficiency Activates Endothelial Cell and Leukocyte Adhesion Mediated via the TGFβ/NADPH Oxidases/ROS Signaling Pathway
by Rajesh Parsanathan and Sushil K. Jain
Int. J. Mol. Sci. 2020, 21(20), 7474; https://doi.org/10.3390/ijms21207474 - 10 Oct 2020
Cited by 18 | Viewed by 7189
Abstract
Glucose-6-phosphate dehydrogenase (G6PD) deficiency, the most common genetic inherited trait among humans, affects ~7% of the global population, and is associated with excess risk of cardiovascular disease (CVD). Transforming growth factor-β (TGF-β) regulates immune function, proliferation, epithelial-mesenchymal transition, fibrosis, cancer, and vascular dysfunction. [...] Read more.
Glucose-6-phosphate dehydrogenase (G6PD) deficiency, the most common genetic inherited trait among humans, affects ~7% of the global population, and is associated with excess risk of cardiovascular disease (CVD). Transforming growth factor-β (TGF-β) regulates immune function, proliferation, epithelial-mesenchymal transition, fibrosis, cancer, and vascular dysfunction. This study examined whether G6PD deficiencies can alter TGF-β-mediated NADPH oxidases (NOX) and cell adhesion molecules (CAM) in human aortic endothelial cells (HAEC). Results show that treatment with high glucose and the saturated free fatty acid palmitate significantly downregulated G6PD; in contrast, mRNA levels of TGF-β components, NOX and its activity, and reactive oxygen species (ROS) were significantly upregulated in HAEC. The expression levels of TGF-β and its receptors, NOX and its activity, and ROS were significantly higher in HG-exposed G6PD-deficient cells (G6PD siRNA) compared to G6PD-normal cells. The protein levels of adhesion molecules (ICAM-1 and VCAM-1) and inflammatory cytokines (MCP-1 and TNF) were significantly increased in HG-exposed G6PD-deficient cells compared to G6PD-normal cells. The adherence of monocytes (SC cells) to HAEC was significantly elevated in HG-treated G6PD-deficient cells compared to control cells. Pharmacological inhibition of G6PD enhances ROS, NOX and its activity, and endothelial monocyte adhesion; these effects were impeded by NOX inhibitors. The inhibition of TGF-β prevents NOX2 and NOX4 mRNA expression and activity, ROS, and adhesion of monocytes to HAEC. L-Cysteine ethyl ester (cell-permeable) suppresses the mRNA levels of TGF-β and its receptors, along with NOX2 and NOX4, and decreases NOX activity, ROS, and adhesion of monocytes to HAEC. This suggests that G6PD deficiency promotes TGF-β/NADPH oxidases/ROS signaling, the expression of ICAM-1 and VCAM-1, and the adhesion of leukocytes to the endothelial monolayer, which can contribute to a higher risk for CVD. Full article
(This article belongs to the Special Issue Endothelial Dysfunction: Pathophysiology and Molecular Mechanisms 2.0)
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Review

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17 pages, 773 KiB  
Review
The Contribution of Endothelial Dysfunction in Systemic Injury Subsequent to SARS-Cov-2 Infection
by Jessica Maiuolo, Rocco Mollace, Micaela Gliozzi, Vincenzo Musolino, Cristina Carresi, Sara Paone, Miriam Scicchitano, Roberta Macrì, Saverio Nucera, Francesca Bosco, Federica Scarano, Maria Caterina Zito, Stefano Ruga, Annamaria Tavernese and Vincenzo Mollace
Int. J. Mol. Sci. 2020, 21(23), 9309; https://doi.org/10.3390/ijms21239309 - 6 Dec 2020
Cited by 21 | Viewed by 4483
Abstract
SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) infection is associated, alongside with lung infection and respiratory disease, to cardiovascular dysfunction that occurs at any stage of the disease. This includes ischemic heart disease, arrhythmias, and cardiomyopathies. The common pathophysiological link between SARS-CoV-2 infection [...] Read more.
SARS-CoV-2 (Severe Acute Respiratory Syndrome Coronavirus 2) infection is associated, alongside with lung infection and respiratory disease, to cardiovascular dysfunction that occurs at any stage of the disease. This includes ischemic heart disease, arrhythmias, and cardiomyopathies. The common pathophysiological link between SARS-CoV-2 infection and the cardiovascular events is represented by coagulation abnormalities and disruption of factors released by endothelial cells, which contribute in maintaining the blood vessels into an anti-thrombotic state. Thus, early alteration of the functionality of endothelial cells, which may be found soon after SARS-CoV-2 infection, seems to represent the major target of a SARS CoV-2 disease state and accounts for the systemic vascular dysfunction that leads to a detrimental effect in terms of hospitalization and death accompanying the disease. In particular, the molecular interaction of SARS-CoV-2 with the ACE2 receptor located in the endothelial cell surface, either at the pulmonary and systemic level, leads to early impairment of endothelial function, which, in turn, is followed by vascular inflammation and thrombosis of peripheral blood vessels. This highlights systemic hypoxia and further aggravates the vicious circle that compromises the development of the disease, leading to irreversible tissue damage and death of people with SARS CoV-2 infection. The review aims to assess some recent advances to define the crucial role of endothelial dysfunction in the pathogenesis of vascular complications accompanying SARS-CoV-2 infection. In particular, the molecular mechanisms associated with the interaction of SARS CoV-2 with the ACE2 receptor located on the endothelial cells are highlighted to support its role in compromising endothelial cell functionality. Finally, the consequences of endothelial dysfunction in enhancing pro-inflammatory and pro-thrombotic effects of SARS-CoV-2 infection are assessed in order to identify early therapeutic interventions able to reduce the impact of the disease in high-risk patients. Full article
(This article belongs to the Special Issue Endothelial Dysfunction: Pathophysiology and Molecular Mechanisms 2.0)
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