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Endothelial Inflammation and Cardiovascular Dysfunction: Oxidative, Nitrosative and Reticulum Stress

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A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (15 November 2022) | Viewed by 10181

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Special Issue Editors

Dr. Amarylis Claudine Bonito A. Wanschel

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Guest Editor

Department of Clinical Sciences and Pharmacy, High Point University, High Point, NC, USA
Interests: intermediate metabolite signaling on: intracardiac cell-cell cross-talk between cardiomyocytes and non-cardiomyocytes; metabolomic signaling; spatial metabolomics; metabolite-protein interactions; post-translational modifications by intermediate metabolites; endoplasmic reticulum stress; oxidative stress; nitrosative stress
Special Issues, Collections and Topics in MDPI journals

Dr. Ana Iochabel Soares Moretti

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Guest Editor

State Government Employee Medical Assistance Institute (IAMSPE), Health Sciences Program, Sao Paulo, SP 04029-000, Brazil
Interests: endothelial cell dysfunction; oxidative stress; protein disulfide isomerase; endoplasmic reticulum stress; unfolded protein response

Dr. Alessandro Gonzalez Salerno

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Guest Editor

Interdisciplinary Stem Cell Institute (ISCI), Miller School of Medicine, University of Miami, Miami, FL 33136, USA
Interests: cardiomyocytes; lipid metabolism; dyslipidemia; heart failure; cell therapy

Special Issue Information

Dear Colleagues,

Endothelial dysfunction is a hallmark of, and the link to, several cardiovascular diseases. At the outset, in considering the mechanisms of endothelial dysfunction and activation, excessive generation of reactive oxygen (ROS) and nitrogen species (RNS) is a key protagonist. ROS and RNS overproduction by a set of enzymes from nitric oxide (NO) synthase and NADPH oxidase families, among others, are commonly involved in cellular damage and CVD development. Furthermore, the disruption of cell homeostasis often affects their inflammatory phenotype and most likely leads to disturbances in the protein synthesis machinery that evokes or amplifies endoplasmatic reticulum stress (ERE) and unfolded protein response (UPR). The presence of ERE/UPR increases oxidative/nitrosative stresses, consequently boosting cell impairment. Therefore, this Research Topic postulates a primary role for endothelial cell dysfunction in inciting CVD and the underlying stress in cardiomyocytes and leukocytes to recapitulate the range of features ultimately found in cardiovascular pathologies. Even our understanding of the initiation factors that preceded CVD, drivers, such as hyperglycemia, hypertension, dyslipidemia, and SARS-CoV-2 infection, as well as their association during this process, is still limited. The aim of this Topical Collection of Biomolecules is to unravel and highlight fundamental pathophysiological mechanisms and evidence-based therapies in CVD.

Dr. Amarylis Claudine Bonito A. Wanschel
Dr. Ana Iochabel Soares Moretti
Dr. Alessandro Gonzalez Salerno
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. Biomolecules is an international peer-reviewed open access monthly 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

endothelium
cardiovascular disease
nitric oxide
macrophage
atherosclerosis
diabetes

Published Papers (3 papers)

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Research

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12 pages, 1435 KiB

Open AccessArticle

Desmopressin Stimulates Nitric Oxide Production in Human Lung Microvascular Endothelial Cells

by Bianca Maria Rotoli, Rossana Visigalli, Francesca Ferrari, Marianna Ranieri, Grazia Tamma, Valeria Dall’Asta and Amelia Barilli

Biomolecules 2022, 12(3), 389; https://0-doi-org.brum.beds.ac.uk/10.3390/biom12030389 - 2 Mar 2022

Cited by 3 | Viewed by 2437

Abstract

Desmopressin (dDAVP) is the best characterized analogue of vasopressin, the endocrine regulator of water balance endowed with potent vasoconstrictive effects. Despite the use of dDAVP in clinical practice, ranging from the treatment of nephrogenic diabetes insipidus to bleeding disorders, much remains to be understood about the impact of the drug on endothelial phenotype. The aim of this study was, thus, to evaluate the effects of desmopressin on the viability and function of human pulmonary microvascular endothelial cells (HLMVECs). The results obtained demonstrate that the vasopressor had no cytotoxic effect on the endothelium; similarly, no sign of endothelial activation was induced by dDAVP, indicated by the lack of effect on the expression of inflammatory cytokines and adhesion molecules. Conversely, the drug significantly stimulated the production of nitric oxide (NO) and the expression of the inducible isoform of nitric oxide synthase, NOS2/iNOS. Since the intracellular level of cAMP also increased, we can hypothesize that NO release is consequent to the activation of the vasopressin receptor 2 (V2R)/guanylate cyclase (Gs)/cAMP axis. Given the multifaceted role of NOS2-deriving NO for many physio-pathological conditions, the meanings of these findings in HLMVECs appears intriguing and deserves to be further addressed. Full article

(This article belongs to the Special Issue Endothelial Inflammation and Cardiovascular Dysfunction: Oxidative, Nitrosative and Reticulum Stress)

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10 pages, 1854 KiB

Open AccessArticle

Association of Circulating miR-145-5p and miR-let7c and Atherosclerotic Plaques in Hypertensive Patients

by Eduarda O. Z. Minin, Layde R. Paim, Elisangela C. P. Lopes, Larissa C. M. Bueno, Luís F. R. S. Carvalho-Romano, Edmilson R. Marques, Camila F. L. Vegian, José A. Pio-Magalhães, Otavio R. Coelho-Filho, Andrei C. Sposito, José R. Matos-Souza, Wilson Nadruz and Roberto Schreiber

Biomolecules 2021, 11(12), 1840; https://0-doi-org.brum.beds.ac.uk/10.3390/biom11121840 - 7 Dec 2021

Cited by 4 | Viewed by 2328

Abstract

Aim: Hypertension is a strong risk factor for atherosclerosis. Increased carotid intima-media thickness (cIMT) and carotid plaques are considered subclinical markers of atherosclerosis. This study aimed at evaluating the serum expression of miRNAs previously related to adverse vascular remodeling and correlating them with carotid plaques and cIMT in hypertensive patients. Methods: We cross-sectionally evaluated the clinical and carotid characteristics as well as serum expression of miR-145-5p, miR-let7c, miR-92a, miR-30a and miR-451 in 177 hypertensive patients. Carotid plaques and cIMT were evaluated by ultrasound, and the expression of selected miRNAs was evaluated by a quantitative polymerase chain reaction. Results: Among all participants (age = 60.6 ± 10.7 years, 43% males), there were 59% with carotid plaques. We observed an increased expression of miR-145-5p (Fold Change = 2.0, p = 0.035) and miR-let7c (Fold Change = 3.8, p = 0.045) in participants with atherosclerotic plaque when compared to those without plaque. In the logistic regression analysis adjusted for relevant covariates, these miRNAs showed a stronger association with carotid plaques (miR-145-5p: Beta ± SE = 0.050 ± 0.020, p = 0.016 and miR-let7c: Beta ± SE = 0.056 ± 0.019, p = 0.003). Conclusions: Hypertensive patients with carotid plaques have an increased expression of miR-145-5p and miR-let7c, suggesting a potential role of these miRNAs as a biomarker for subclinical atherosclerosis in hypertensive individuals. Full article

(This article belongs to the Special Issue Endothelial Inflammation and Cardiovascular Dysfunction: Oxidative, Nitrosative and Reticulum Stress)

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Review

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26 pages, 4898 KiB

Open AccessEditor’s ChoiceReview

The Mechanisms of Restenosis and Relevance to Next Generation Stent Design

by Jessie Clare, Justin Ganly, Christina A. Bursill, Huseyin Sumer, Peter Kingshott and Judy B. de Haan

Biomolecules 2022, 12(3), 430; https://0-doi-org.brum.beds.ac.uk/10.3390/biom12030430 - 10 Mar 2022

Cited by 23 | Viewed by 4606

Abstract

Stents are lifesaving mechanical devices that re-establish essential blood flow to the coronary circulation after significant vessel occlusion due to coronary vessel disease or thrombolytic blockade. Improvements in stent surface engineering over the last 20 years have seen significant reductions in complications arising due to restenosis and thrombosis. However, under certain conditions such as diabetes mellitus (DM), the incidence of stent-mediated complications remains 2–4-fold higher than seen in non-diabetic patients. The stents with the largest market share are designed to target the mechanisms behind neointimal hyperplasia (NIH) through anti-proliferative drugs that prevent the formation of a neointima by halting the cell cycle of vascular smooth muscle cells (VSMCs). Thrombosis is treated through dual anti-platelet therapy (DAPT), which is the continual use of aspirin and a P2Y₁₂ inhibitor for 6–12 months. While the most common stents currently in use are reasonably effective at treating these complications, there is still significant room for improvement. Recently, inflammation and redox stress have been identified as major contributing factors that increase the risk of stent-related complications following percutaneous coronary intervention (PCI). The aim of this review is to examine the mechanisms behind inflammation and redox stress through the lens of PCI and its complications and to establish whether tailored targeting of these key mechanistic pathways offers improved outcomes for patients, particularly those where stent placement remains vulnerable to complications. In summary, our review highlights the most recent and promising research being undertaken in understanding the mechanisms of redox biology and inflammation in the context of stent design. We emphasize the benefits of a targeted mechanistic approach to decrease all-cause mortality, even in patients with diabetes. Full article

(This article belongs to the Special Issue Endothelial Inflammation and Cardiovascular Dysfunction: Oxidative, Nitrosative and Reticulum Stress)

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