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Biomedicines
Special Issues
Oxidative Stress and Cardiovascular Diseases
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Oxidative Stress and Cardiovascular Diseases

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (31 August 2023) | Viewed by 2878

Special Issue Editor

Dr. Cristiana Bustea

E-Mail Website
Guest Editor
Department of Preclinical Disciplines, Faculty of Medicine and Pharmacy, University of Oradea, 410073 Oradea, Romania
Interests: cardiovascular disease; pathophysiology; oxidative stress; inflammation; hemostasis; diabetes mellitus
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Oxidative stress has been widely recognized as an important risk factor for cardiovascular diseases with an atherosclerotic component, such as hypertension or acute coronary syndromes. The pathophysiological mechanisms by which oxidative stress leads to the induction of the pro-atherosclerotic process include: the inactivation of nitric oxide, the activation of pro-inflammatory pathways such as nuclear factor-kappa B (NF-κB) pathway, the increase in macrophage infiltration and cell proliferation, and the generation of oxidatively modified low-density lipoproteins (OxLDL). Much remains to be explored regarding the association between oxidative stress and heart failure as recent data demonstrate that oxidative stress promotes intracellular signaling associated with myocardial hypertrophy. Oxidative stress can also increase the risk for arrhythmias as it leads to aberrant intracellular Ca2+ release.

The present Special Issue has the purpose to analyze novel correlations between oxidative stress and cardiovascular disease and modalities to reduce the impact of oxidative stress on the heart function. Numerous pharmacological and nutritional approaches have proven efficient to alleviate this process such as xanthine oxidase inhibitors, statins, fibrates, glucagon-like peptide-1 (GLP-1) agonists, polyunsaturated fatty acids, antioxidant vitamins, and flavonoids.

Therefore, we cordially invite all of you to take part in this project by submitting original research or review articles within this field. From cellular and molecular abnormalities caused by oxidative stress resulting in cardiac dysfunction to antioxidant therapies impacting cardiovascular diseases, all papers that bring forward new opinions and studies are warmly welcome in this Special Issue.

Dr. Cristiana Bustea
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. Biomedicines 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 2600 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

  • oxidative stress
  • cardiovascular diseases
  • reactive oxygen species
  • heart failure
  • atrial fibrillation
  • atherosclerosis antioxidants

Published Papers (2 papers)

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Research

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16 pages, 12696 KiB  
Article
Persistent Hypoxia with Intermittent Aggravation Causes Imbalance in Smad3/Myocardin-Related Transcription Factor Signaling with Consequent Endothelial Senescence and Pulmonary Arterial Remodeling
by Jiaxin Hu, Prachi Singh, Jingrui Li, Jing Zhang, Fei Li, Hehe Zhang and Jiang Xie
Biomedicines 2023, 11(9), 2351; https://doi.org/10.3390/biomedicines11092351 - 23 Aug 2023
Cited by 1 | Viewed by 858
Abstract
Loss of Smad3 and the consequent activation of myocardin-related transcription factor (MRTF) are associated with vascular pathologies. This study aimed to examine the impact of persistent hypoxia with intermittent aggravation (PI hypoxia) on cellular senescence and pulmonary arterial remodeling mediated by the Smad3/MRTF [...] Read more.
Loss of Smad3 and the consequent activation of myocardin-related transcription factor (MRTF) are associated with vascular pathologies. This study aimed to examine the impact of persistent hypoxia with intermittent aggravation (PI hypoxia) on cellular senescence and pulmonary arterial remodeling mediated by the Smad3/MRTF imbalance. We examined the effects of PI hypoxia on the Smad3/MRTF pathway and cellular senescence using human pulmonary artery endothelial cells (HPAECs) and in vivo studies in rats. The senescent degree was evaluated using β-galactosidase staining, p16 quantitation and the measurement of senescence-associated secretory phenotype. Structural data in the pathological analysis of pulmonary artery remodeling were collected. Compared to the control, HPAECs and pulmonary tissue from rats exposed to PI hypoxia showed a significantly higher senescent degree, lower expression of Smad3, and higher MRTF levels. The overexpression of Smad3 significantly mitigated HPAECs senescence in vitro. Further, treatment with CCG-203971, which inhibits MRTF, increased Smad3 levels and reduced β-galactosidase positive cells in rat lung tissue. This intervention also alleviated PI hypoxia-induced pathological changes, including remodeling indices of pulmonary arterial thickening, muscularization, and collagen formation. In conclusion, imbalanced Smad3/MRTF signaling is linked to PI hypoxia-induced senescence and pulmonary arterial remodeling, making it a potential therapeutic target for patients with sleep apnea and chronic obstructive pulmonary disease. Full article
(This article belongs to the Special Issue Oxidative Stress and Cardiovascular Diseases)
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Review

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15 pages, 1205 KiB  
Review
A Review of the Relationship between the Immune Response, Inflammation, Oxidative Stress, and the Pathogenesis of Sickle Cell Anaemia
by Florence Ifechukwude Aboderin, Taofeeq Oduola, Glenda Mary Davison and Oluwafemi Omoniyi Oguntibeju
Biomedicines 2023, 11(9), 2413; https://doi.org/10.3390/biomedicines11092413 - 29 Aug 2023
Cited by 2 | Viewed by 1661
Abstract
Sickle cell anaemia (SCD) is a life-threatening haematological disorder which is predominant in sub-Saharan Africa and is triggered by a genetic mutation of the β-chain haemoglobin gene resulting in the substitution of glutamic acid with valine. This mutation leads to the production of [...] Read more.
Sickle cell anaemia (SCD) is a life-threatening haematological disorder which is predominant in sub-Saharan Africa and is triggered by a genetic mutation of the β-chain haemoglobin gene resulting in the substitution of glutamic acid with valine. This mutation leads to the production of an abnormal haemoglobin molecule called haemoglobin S (HbS). When deoxygenated, haemoglobin S (HbS) polymerises and results in a sickle-shaped red blood cell which is rigid and has a significantly shortened life span. Various reports have shown a strong link between oxidative stress, inflammation, the immune response, and the pathogenesis of sickle cell disease. The consequence of these processes leads to the development of vasculopathy (disease of the blood vessels) and several other complications. The role of the immune system, particularly the innate immune system, in the pathogenesis of SCD has become increasingly clear in recent years of research; however, little is known about the roles of the adaptive immune system in this disease. This review examines the interaction between the immune system, inflammation, oxidative stress, blood transfusion, and their effects on the pathogenesis of sickle cell anaemia. Full article
(This article belongs to the Special Issue Oxidative Stress and Cardiovascular Diseases)
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