Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
10.6
6.0
Journals
Antioxidants
Special Issues
Role of Oxidative Stress in Cardiac Remodeling and Heart Failure—2nd...
share announcement

Role of Oxidative Stress in Cardiac Remodeling and Heart Failure—2nd Edition

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: closed (15 September 2024) | Viewed by 7185

Special Issue Editor

Dr. Marina Politi Okoshi

E-Mail Website
Guest Editor
Department of Internal Medicine, Botucatu Medical School, Sao Paulo State University, UNESP, Botucatu 18618-687, SP, Brazil
Interests: heart failure; skeletal muscle; cardiac remodeling; physical exercise; cell signaling; ventricular function
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Our previous Special Issue on the “Role of Oxidative Stress in Cardiac Remodeling and Heart Failure” (https://www.mdpi.com/journal/antioxidants/special_issues/Oxidative_Heart), published in the 2022 volume of Antioxidants, received an overwhelming number of submissions and was a successful compilation of research and review articles. As this is a rapidly evolving topic, we would like to further explore the role of oxidative stress in cardiac remodeling and heart failure with a follow-up Special Issue for the year 2024.

Cardiac remodeling is defined as molecular, cellular, and interstitial cardiac changes that clinically manifest as changes in the size, shape, and function of the heart. Cardiac failure is the final pathway of many cardiac diseases and presents a major public health issue due to its poor prognosis and high prevalence, morbidity, and mortality. Oxidative stress is characterized by an increased ratio between oxygen radical production and scavenging capacity. Although at low levels, reactive oxygen species play a role in intracellular signaling pathways, at higher levels, they may induce cellular injury, dysfunction, and death. Clinical and experimental studies have shown that oxidative stress is increased in the myocardium and at a systemic level during heart failure, and in the myocardium, increased oxidative stress may result from injured myocytes and may induce additional lesions to myocardial cells, therefore forming a vicious cycle. Despite extensive studies, the molecular pathways involved in heart failure-associated oxidative stress are still not completely understood. 

This Special Issue is dedicated to reviews and original research regarding in vitro, animal experiments, and clinical studies about the mechanisms underlying the role of increased oxidative stress in cardiac remodeling and heart failure pathophysiology, clinical manifestations, novel targets, and pharmacological and non-pharmacological treatment.

Dr. Marina Politi Okoshi
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. Antioxidants 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 2900 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
  • cardiac failure
  • signaling pathways
  • remodeling
  • left ventricular dysfunction

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (4 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

15 pages, 3552 KiB  
Article
Mitigating Doxorubicin-Induced Cardiotoxicity through Quercetin Intervention: An Experimental Study in Rats
by Patricia Lorena Dulf, Camelia Alexandra Coadă, Adrian Florea, Remus Moldovan, Ioana Baldea, Daniel Vasile Dulf, Dan Blendea and Adriana Gabriela Filip
Antioxidants 2024, 13(9), 1068; https://doi.org/10.3390/antiox13091068 - 31 Aug 2024
Cited by 1 | Viewed by 1124
Abstract
Doxorubicin (DOX) is an effective anticancer drug, but its use is limited by dose-dependent heart toxicity. Quercetin is a natural antioxidant frequently studied for its beneficial properties. Moreover, a wide range of dietary supplements are available for human use. This in vivo study [...] Read more.
Doxorubicin (DOX) is an effective anticancer drug, but its use is limited by dose-dependent heart toxicity. Quercetin is a natural antioxidant frequently studied for its beneficial properties. Moreover, a wide range of dietary supplements are available for human use. This in vivo study aimed to explore the potential cardioprotective effects of quercetin in chronic DOX treatment. A total of 32 Wistar rats were randomly divided into four groups: control, DOX, DOX/Q-50, and DOX/Q-100, treated with saline, 2.5 mg/kg body-weight DOX, 2.5 mg/kg body-weight DOX + 50 mg quercetin, and 2.5 mg/kg body-weight DOX + 100 mg quercetin, respectively, for two weeks. Rats were monitored using cardiac ultrasound (US) and markers for cardiac injury. Oxidative damage and ultrastructural changes in the heart were investigated. Chronic DOX treatment led to a decline in cardiac function and elevated values of NT pro-BNP, troponin I, and CK-MB. Quercetin treatment slightly improved certain US parameters, and normalized serum NT pro-BNP levels. Furthermore, DOX-induced SOD1 depletion with consequent Nrf2 activation and DNA damage as shown by an increase in γH2AX and 8HOdG. Quercetin treatment alleviated these alterations. Oral administration of quercetin alleviated serum markers associated with DOX-induced cardiotoxicity. Furthermore, it exhibited a favorable impact on the cardiac US parameters. This suggests that quercetin may have potential cardioprotective properties. Full article
(This article belongs to the Special Issue Role of Oxidative Stress in Cardiac Remodeling and Heart Failure—2nd Edition)
►▼ Show Figures

Graphical abstract

15 pages, 5571 KiB  
Article
Alterations in Mitochondrial Oxidative Phosphorylation System: Relationship of Complex V and Cardiac Dysfunction in Human Heart Failure
by Isaac Giménez-Escamilla, Carlota Benedicto, Lorena Pérez-Carrillo, Marta Delgado-Arija, Irene González-Torrent, Roger Vilchez, Luis Martínez-Dolz, Manuel Portolés, Estefanía Tarazón and Esther Roselló-Lletí
Antioxidants 2024, 13(3), 285; https://doi.org/10.3390/antiox13030285 - 26 Feb 2024
Cited by 1 | Viewed by 2056
Abstract
Heart failure (HF) is a disease related to bioenergetic mitochondrial abnormalities. However, the whole status of molecules involved in the oxidative phosphorylation system (OXPHOS) is unknown. Therefore, we analyzed the OXPHOS transcriptome of human cardiac tissue by RNA-seq analyses (mRNA n = 36; [...] Read more.
Heart failure (HF) is a disease related to bioenergetic mitochondrial abnormalities. However, the whole status of molecules involved in the oxidative phosphorylation system (OXPHOS) is unknown. Therefore, we analyzed the OXPHOS transcriptome of human cardiac tissue by RNA-seq analyses (mRNA n = 36; ncRNA n = 30) in HF patients (ischemic cardiomyopathy (ICM) and dilated cardiomyopathy (DCM)) and control subjects. We detected 28 altered genes in these patients, highlighting greater deregulation in ICM. Specifically, we found a general overexpression of complex V (ATP synthase) elements, among them, ATP5I (ICM, FC = 2.04; p < 0.01), ATP5MJ (ICM, FC = 1.33, p < 0.05), and ATP5IF1 (ICM, FC = 1.81; p < 0.001), which presented a significant correlation with established echocardiographic parameters of cardiac remodeling and ventricular function as follows: left ventricular end-systolic (p < 0.01) and end-diastolic (p < 0.01) diameters, and ejection fraction (p < 0.05). We also detected an increase in ATP5IF1 protein levels (ICM, FC = 1.75; p < 0.01) and alterations in the microRNA expression levels of miR-208b-3p (ICM, FC = −1.44, p < 0.001), miR-483-3p (ICM, FC = 1.37, p < 0.01), regulators of ATP5I. Therefore, we observed the deregulation of the OXPHOS transcriptome in ICM patients, highlighting the overexpression of complex V and its relationship with cardiac remodeling and function. Full article
(This article belongs to the Special Issue Role of Oxidative Stress in Cardiac Remodeling and Heart Failure—2nd Edition)
►▼ Show Figures

Graphical abstract

18 pages, 3085 KiB  
Article
Altered MicroRNA Maturation in Ischemic Hearts: Implication of Hypoxia on XPO5 and DICER1 Dysregulation and RedoximiR State
by Lorena Pérez-Carrillo, Isaac Giménez-Escamilla, María García-Manzanares, Juan Carlos Triviño, Sandra Feijóo-Bandín, Alana Aragón-Herrera, Francisca Lago, Luis Martínez-Dolz, Manuel Portolés, Estefanía Tarazón and Esther Roselló-Lletí
Antioxidants 2023, 12(7), 1337; https://doi.org/10.3390/antiox12071337 - 24 Jun 2023
Viewed by 1697
Abstract
Ischemic cardiomyopathy (ICM) is associated with abnormal microRNA expression levels that involve an altered gene expression profile. However, little is known about the underlying causes of microRNA disruption in ICM and whether microRNA maturation is compromised. Therefore, we focused on microRNA maturation defects [...] Read more.
Ischemic cardiomyopathy (ICM) is associated with abnormal microRNA expression levels that involve an altered gene expression profile. However, little is known about the underlying causes of microRNA disruption in ICM and whether microRNA maturation is compromised. Therefore, we focused on microRNA maturation defects analysis and the implication of the microRNA biogenesis pathway and redox-sensitive microRNAs (redoximiRs). Transcriptomic changes were investigated via ncRNA-seq (ICM, n = 22; controls, n = 8) and mRNA-seq (ICM, n = 13; control, n = 10). The effect of hypoxia on the biogenesis of microRNAs was evaluated in the AC16 cell line. ICM patients showed a reduction in microRNA maturation compared to control (4.30 ± 0.94 au vs. 5.34 ± 1.07 au, p ˂ 0.05), accompanied by a deregulation of the microRNA biogenesis pathway: a decrease in pre-microRNA export (XPO5, FC = −1.38, p ˂ 0.05) and cytoplasmic processing (DICER, FC = −1.32, p ˂ 0.01). Both processes were regulated by hypoxia in AC16 cells (XPO5, FC = −1.65; DICER1, FC = −1.55; p ˂ 0.01; Exportin-5, FC = −1.81; Dicer, FC = −1.15; p ˂ 0.05). Patients displayed deregulation of several redoximiRs, highlighting miR-122-5p (FC = −2.41, p ˂ 0.001), which maintained a good correlation with the ejection fraction (r = 0.681, p ˂ 0.01). We evidenced a decrease in microRNA maturation mainly linked to a decrease in XPO5-mediated pre-microRNA export and DICER1-mediated processing, together with a general effect of hypoxia through deregulation of biogenesis pathway and the redoximiRs. Full article
(This article belongs to the Special Issue Role of Oxidative Stress in Cardiac Remodeling and Heart Failure—2nd Edition)
►▼ Show Figures

Figure 1

Review

Jump to: Research

14 pages, 755 KiB  
Review
The Role of Omega-3 in Attenuating Cardiac Remodeling and Heart Failure through the Oxidative Stress and Inflammation Pathways
by Taline Lazzarin, Danilo Martins, Raquel S. Ballarin, Marina G. Monte, Marcos F. Minicucci, Bertha F. Polegato and Leonardo Zornoff
Antioxidants 2023, 12(12), 2067; https://doi.org/10.3390/antiox12122067 - 1 Dec 2023
Cited by 1 | Viewed by 1726
Abstract
Cardiac remodeling is defined as molecular, cellular, and interstitial changes that manifest clinically as alterations in the size, shape, and function of the heart. Despite the pharmacological approaches, cardiac remodeling-related mortality rates remain high. Therefore, other therapeutic options are being increasingly studied. This [...] Read more.
Cardiac remodeling is defined as molecular, cellular, and interstitial changes that manifest clinically as alterations in the size, shape, and function of the heart. Despite the pharmacological approaches, cardiac remodeling-related mortality rates remain high. Therefore, other therapeutic options are being increasingly studied. This review highlights the role of omega-3 as an adjunctive therapy to attenuate cardiac remodeling, with an emphasis on its antioxidant and anti-inflammatory actions. Full article
(This article belongs to the Special Issue Role of Oxidative Stress in Cardiac Remodeling and Heart Failure—2nd Edition)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-4
Back to TopTop