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Biomolecules
Special Issues
Endothelial Inflammation and Cardiovascular Dysfunction: Oxidative, Nitrosative and Reticulum Stress
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Endothelial Inflammation and Cardiovascular Dysfunction: Oxidative, Nitrosative and Reticulum Stress

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 12323

Special Issue Editors

Dr. Amarylis Claudine Bonito A. Wanschel

E-Mail Website
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

E-Mail Website
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

E-Mail Website
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

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Keywords

  • endothelium
  • cardiovascular disease
  • nitric oxide
  • macrophage
  • atherosclerosis
  • diabetes

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Published Papers (3 papers)

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Research

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12 pages, 1435 KiB  
Article
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://doi.org/10.3390/biom12030389 - 2 Mar 2022
Cited by 4 | Viewed by 2899
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 [...] Read more.
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  
Article
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://doi.org/10.3390/biom11121840 - 7 Dec 2021
Cited by 6 | Viewed by 2643
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 [...] Read more.
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  
Review
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://doi.org/10.3390/biom12030430 - 10 Mar 2022
Cited by 31 | Viewed by 5893
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 [...] Read more.
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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