Understanding Oxidative Stress in Cardiovascular Disorders

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 30 November 2024 | Viewed by 1094

Special Issue Editors


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Department of Experimental and Clinical Biomedical Sciences "Mario Serio", University of Firenze, 50121 Firenze, Italy
Interests: thrombosis; fibrinogen; oxidative stress; protein structure
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Department of Biomedical, Experimental and Clinical Sciences “Mario Serio”, University of Florence, Viale Morgagni 50, 50134 Florence, Italy
Interests: redox markers; antioxidant capacity; post-translational oxidative modification; ROS sources
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

We are pleased to introduce our forthcoming Special Issue, which will delve into the critical relationship between oxidative stress and cardiovascular diseases (CVDs). Oxidative stress, characterized by an imbalance between reactive oxygen species (ROS) production and the body's antioxidant defenses, has emerged as a central player in the pathogenesis and progression of various cardiovascular disorders.

This Special Issue aims to illuminate the intricate mechanisms through which oxidative stress contributes to the development and exacerbation of CVDs, including atherosclerosis, hypertension, myocardial infarction, and heart failure. By unraveling the involved molecular pathways, we seek to identify novel therapeutic targets and interventions to combat these debilitating conditions.

Contributions to this Special Issue will explore the multifaceted roles of oxidative stress in CVDs, from its impact on endothelial dysfunction and vascular inflammation to its involvement in myocardial remodeling and cardiac dysfunction. Researchers are encouraged to investigate both the upstream triggers of oxidative stress, such as dyslipidemia, hypertension, and diabetes, as well as the downstream consequences, including the oxidative modification of lipids, proteins, and DNA.

Furthermore, we welcome studies that explore the potential of antioxidant therapies and lifestyle interventions in mitigating oxidative stress and preventing CVDs. From preclinical research elucidating the efficacy of novel antioxidants to clinical trials evaluating the cardiovascular benefits of dietary modifications and exercise interventions, this Special Issue aims to provide a comprehensive overview of current strategies for managing oxidative stress in the context of cardiovascular health.

In summary, this Special Issue seeks to advance our understanding of the complex interplay between oxidative stress and cardiovascular diseases. By identifying key molecular targets and therapeutic strategies, we aim to pave the way for innovative approaches to prevent, diagnose, and treat CVDs, ultimately improving patient outcomes and reducing the global burden of cardiovascular morbidity and mortality.

Dr. Matteo Becatti
Dr. Claudia Fiorillo
Guest Editors

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Keywords

  • oxidative stress
  • reactive oxygen species
  • cardiovascular diseases
  • antioxidants
  • diet
  • exercise

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Published Papers (1 paper)

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Research

15 pages, 2453 KiB  
Article
TNFα Induces DNA and Histone Hypomethylation and Pulmonary Artery Smooth Muscle Cell Proliferation Partly via Excessive Superoxide Formation
by Patrick Crosswhite and Zhongjie Sun
Antioxidants 2024, 13(6), 677; https://doi.org/10.3390/antiox13060677 - 31 May 2024
Viewed by 726
Abstract
Objective: The level of tumor necrosis factor-α (TNF-α) is upregulated during the development of pulmonary vascular remodeling and pulmonary hypertension. A hallmark of pulmonary arterial (PA) remodeling is the excessive proliferation of PA smooth muscle cells (PASMCs). The purpose of this study is [...] Read more.
Objective: The level of tumor necrosis factor-α (TNF-α) is upregulated during the development of pulmonary vascular remodeling and pulmonary hypertension. A hallmark of pulmonary arterial (PA) remodeling is the excessive proliferation of PA smooth muscle cells (PASMCs). The purpose of this study is to investigate whether TNF-α induces PASMC proliferation and explore the potential mechanisms. Methods: PASMCs were isolated from 8-week-old male Sprague-Dawley rats and treated with 0, 20, or 200 ng/mL TNF-α for 24 or 48 h. After treatment, cell number, superoxide production, histone acetylation, DNA methylation, and histone methylation were assessed. Results: TNF-α treatment increased NADPH oxidase activity, superoxide production, and cell numbers compared to untreated controls. TNF-α-induced PASMC proliferation was rescued by a superoxide dismutase mimetic tempol. TNF-α treatment did not affect histone acetylation at either dose but did significantly decrease DNA methylation. DNA methyltransferase 1 activity was unchanged by TNF-α treatment. Further investigation using QRT-RT-PCR revealed that GADD45-α, a potential mediator of DNA demethylation, was increased after TNF-α treatment. RNAi inhibition of GADD45-α alone increased DNA methylation. TNF-α impaired the epigenetic mechanism leading to DNA hypomethylation, which can be abolished by a superoxide scavenger tempol. TNF-α treatment also decreased H3-K4 methylation. TNF-α-induced PASMC proliferation may involve the H3-K4 demethylase enzyme, lysine-specific demethylase 1 (LSD1). Conclusions: TNF-α-induced PASMC proliferation may be partly associated with excessive superoxide formation and histone and DNA methylation. Full article
(This article belongs to the Special Issue Understanding Oxidative Stress in Cardiovascular Disorders)
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