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Oxidative Stress and Inflammation in Cardiovascular Disease
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Oxidative Stress and Inflammation in Cardiovascular Disease

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 2023) | Viewed by 7382

Special Issue Editor

Dr. Ada Popolo

E-Mail Website
Guest Editor
Department of Pharmacy, University of Salerno, 84084 Fisciano, SA, Italy
Interests: cardiovascular toxicology; calcium homeostasis; clinical pharmacology; oxidative stress; inflammation
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cardiovascular disease is one of the major healthcare problems worldwide. Growing bodies of evidences indicate that oxidative stress and inflammation are intricately linked mechanisms and are significant drivers in the development and progression of cardiovascular disease. Indeed, both oxidative stress and inflammation are enhanced in chronic heart failure and are also involved in drug induced-cardiotoxicity. Oxidative stress also causes myocardial tissue damage and inflammation, contributing to heart failure progression, while a subclinical inflammatory state may be caused by heart failure comorbidities such as obesity or diabetes mellitus. The close interaction of inflammation with oxidative stress is corroborated by clinical data reporting an aggravated inflammatory phenotype in the absence of antioxidant defense proteins (e.g., superoxide dismutases, heme oxygenase-1, and glutathione peroxidases) or overexpression of reactive oxygen species producing enzymes (e.g., NADPH oxidases) and a normalization of oxidative stress exerted by antiinflammatory drugs in cardiovascular diseases.

This Special Issue is calling both original articles and reviews providing to the readers of IJMS a comprehensive, deep understanding of our current knowledge on oxidative stress and inflammation in cardiovascular diseases.

Dr. Ada Popolo
Guest Editor

Manuscript Submission Information

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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.

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Keywords

  • oxidative stress
  • inflammation
  • cardiovascular disease
  • cardiotoxicity
  • endothelial dysfunction
  • mitochondrial stress
  • antiinflammatory and antioxidant drug discovery

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Published Papers (3 papers)

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Research

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20 pages, 4900 KiB  
Article
Effects of Zinc on the Right Cardiovascular Circuit in Long-Term Hypobaric Hypoxia in Wistar Rats
by Karem Arriaza, Julio Brito, Patricia Siques, Karen Flores, Stefany Ordenes, Daniel Aguayo, María del Rosario López and Silvia M. Arribas
Int. J. Mol. Sci. 2023, 24(11), 9567; https://doi.org/10.3390/ijms24119567 - 31 May 2023
Cited by 2 | Viewed by 2146
Abstract
Hypobaric hypoxia under chromic conditions triggers hypoxic pulmonary vasoconstriction (HPV) and right ventricular hypertrophy (RVH). The role of zinc (Zn) under hypoxia is controversial and remains unclear. We evaluated the effect of Zn supplementation in prolonged hypobaric hypoxia on HIF2α/MTF-1/MT/ZIP12/PKCε pathway in the [...] Read more.
Hypobaric hypoxia under chromic conditions triggers hypoxic pulmonary vasoconstriction (HPV) and right ventricular hypertrophy (RVH). The role of zinc (Zn) under hypoxia is controversial and remains unclear. We evaluated the effect of Zn supplementation in prolonged hypobaric hypoxia on HIF2α/MTF-1/MT/ZIP12/PKCε pathway in the lung and RVH. Wistar rats were exposed to hypobaric hypoxia for 30 days and randomly allocated into three groups: chronic hypoxia (CH); intermittent hypoxia (2 days hypoxia/2 days normoxia; CIH); and normoxia (sea level control; NX). Each group was subdivided (n = 8) to receive either 1% Zn sulfate solution (z) or saline (s) intraperitoneally. Body weight, hemoglobin, and RVH were measured. Zn levels were evaluated in plasma and lung tissue. Additionally, the lipid peroxidation levels, HIF2α/MTF-1/MT/ZIP12/PKCε protein expression and pulmonary artery remodeling were measured in the lung. The CIH and CH groups showed decreased plasma Zn and body weight and increased hemoglobin, RVH, and vascular remodeling; the CH group also showed increased lipid peroxidation. Zn administration under hypobaric hypoxia upregulated the HIF2α/MTF-1/MT/ZIP12/PKCε pathway and increased RVH in the intermittent zinc group. Under intermittent hypobaric hypoxia, Zn dysregulation could participate in RVH development through alterations in the pulmonary HIF2α/MTF1/MT/ZIP12/PKCε pathway. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Cardiovascular Disease)
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13 pages, 2149 KiB  
Article
Simvastatin Reduces Doxorubicin-Induced Cardiotoxicity: Effects beyond Its Antioxidant Activity
by Michela Pecoraro, Stefania Marzocco, Raffaella Belvedere, Antonello Petrella, Silvia Franceschelli and Ada Popolo
Int. J. Mol. Sci. 2023, 24(8), 7573; https://doi.org/10.3390/ijms24087573 - 20 Apr 2023
Cited by 15 | Viewed by 2122
Abstract
This study aimed to evaluate if Simvastatin can reduce, and/or prevent, Doxorubicin (Doxo)-induced cardiotoxicity. H9c2 cells were treated with Simvastatin (10 µM) for 4 h and then Doxo (1 µM) was added, and the effects on oxidative stress, calcium homeostasis, and apoptosis were [...] Read more.
This study aimed to evaluate if Simvastatin can reduce, and/or prevent, Doxorubicin (Doxo)-induced cardiotoxicity. H9c2 cells were treated with Simvastatin (10 µM) for 4 h and then Doxo (1 µM) was added, and the effects on oxidative stress, calcium homeostasis, and apoptosis were evaluated after 20 h. Furthermore, we evaluated the effects of Simvastatin and Doxo co-treatment on Connexin 43 (Cx43) expression and localization, since this transmembrane protein forming gap junctions is widely involved in cardioprotection. Cytofluorimetric analysis showed that Simvastatin co-treatment significantly reduced Doxo-induced cytosolic and mitochondrial ROS overproduction, apoptosis, and cytochrome c release. Spectrofluorimetric analysis performed by means of Fura2 showed that Simvastatin co-treatment reduced calcium levels stored in mitochondria and restored cytosolic calcium storage. Western blot, immunofluorescence, and cytofluorimetric analyses showed that Simvastatin co-treatment significantly reduced Doxo-induced mitochondrial Cx43 over-expression and significantly increased the membrane levels of Cx43 phosphorylated on Ser368. We hypothesized that the reduced expression of mitochondrial Cx43 could justify the reduced levels of calcium stored in mitochondria and the consequent induction of apoptosis observed in Simvastatin co-treated cells. Moreover, the increased membrane levels of Cx43 phosphorylated on Ser368, which is responsible for the closed conformational state of the gap junction, let us to hypothesize that Simvastatin leads to cell-to-cell communication interruption to block the propagation of Doxo-induced harmful stimuli. Based on these results, we can conclude that Simvastatin could be a good adjuvant in Doxo anticancer therapy. Indeed, we confirmed its antioxidant and antiapoptotic activity, and, above all, we highlighted that Simvastatin interferes with expression and cellular localization of Cx43 that is widely involved in cardioprotection. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Cardiovascular Disease)
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Review

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35 pages, 2594 KiB  
Review
Developing Pharmacological Therapies for Atrial Fibrillation Targeting Mitochondrial Dysfunction and Oxidative Stress: A Scoping Review
by Antônio da Silva Menezes Júnior, Ana Luísa Guedes de França-e-Silva, Joyce Monteiro de Oliveira and Daniela Melo da Silva
Int. J. Mol. Sci. 2024, 25(1), 535; https://doi.org/10.3390/ijms25010535 - 30 Dec 2023
Cited by 6 | Viewed by 2358
Abstract
Atrial fibrillation (AF) is a cardiac arrhythmia caused by electrophysiological anomalies in the atrial tissue, tissue degradation, structural abnormalities, and comorbidities. A direct relationship exists between AF and altered mitochondrial activity resulting from membrane potential loss, contractile dysfunction, or decreased ATP levels. This [...] Read more.
Atrial fibrillation (AF) is a cardiac arrhythmia caused by electrophysiological anomalies in the atrial tissue, tissue degradation, structural abnormalities, and comorbidities. A direct relationship exists between AF and altered mitochondrial activity resulting from membrane potential loss, contractile dysfunction, or decreased ATP levels. This review aimed to elucidate the role of mitochondrial oxidative mechanisms in AF pathophysiology, the impact of mitochondrial oxidative stress on AF initiation and perpetuation, and current therapies. This review followed the Preferred Reporting Items for Systematic Reviews and the Meta-Analysis Extension for Scoping Reviews. PubMed, Excerpta Medica Database, and Scopus were explored until June 2023 using “MESH terms”. Bibliographic references to relevant papers were also included. Oxidative stress is an imbalance that causes cellular damage from excessive oxidation, resulting in conditions such as AF. An imbalance in reactive oxygen species production and elimination can cause mitochondrial damage, cellular apoptosis, and cardiovascular diseases. Oxidative stress and inflammation are intrinsically linked, and inflammatory pathways are highly correlated with the occurrence of AF. AF is an intricate cardiac condition that requires innovative therapeutic approaches. The involvement of mitochondrial oxidative stress in the pathophysiology of AF introduces novel strategies for clinical treatment. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Cardiovascular Disease)
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