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Biomedicines
Special Issues
Oxidative Stress Markers in Cardiomyopathy
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Oxidative Stress Markers in Cardiomyopathy

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

Deadline for manuscript submissions: 31 August 2024 | Viewed by 1971

Special Issue Editors

Dr. Celina Wojciechowska

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Guest Editor
Second Department of Cardiology, Faculty of Medical Sciences in Zabrze, Medical University of Silesia, 40-055 Katowice, Poland
Interests: pulmonary arterial hypertension; heart failure; cardiomyopathy
Dr. Ewa B. Romuk

E-Mail Website
Guest Editor
Department of Biochemistry, School of Medical Sciences in Zabrze, Medical University of Silesia, 40-055 Katowice, Poland
Interests: oxidative stress; redox-related biomarkers; antioxidants; heart failure; cardiomyopathy
Dr. Wojciech Jachec

E-Mail Website
Guest Editor
Department of Cardiology, Slaski Uniwersytet Medyczny w Katowicach, Katowice, Poland
Interests: coronary artery disease; heart failure; cardiac catheterization; cardiomyopathies; chronic heart failure; pulmonary hypertension

Special Issue Information

Dear Colleagues,

Cardiomyopathies are the heterogenous group of the heart muscle disease, characterized by structural and functional alterations in the absence of coronary artery disease, hypertension, and valvular disease. Despite the expanding diagnostic knowledge on the acquired and genetic causes of cardiomyopathies with various morpho functional phenotypes,  their consequences, such as heart failure, arrythmias, and sudden cardiac death, are still a significant problem.

There is no doubt that an imbalance between oxidative and reduction reactions is involved in the pathogenesis of cardiac impairment in various types of cardiomyopathy. Additionally, in heart failure, neuroendocrine activation, mediated by the renin–angiotensin system and the sympathetic nervous system, is a trigger of oxidative stress, and this may contribute to the progression of heart failure. Despite many experimental studies documenting the adverse effects of oxidative stress on the onset and progression of cardiovascular diseases, it is disappointing that antioxidant therapies have not produced the expected benefits. There seems to be much work to be conducted in this field in the age of personalized treatment. We therefore encourage all researchers to publish both experimental and clinical studies on this topic. We also invite experts to share their opinions in review articles.

Dr. Celina Wojciechowska
Dr. Ewa B. Romuk
Dr. Wojciech Jachec
Guest Editors

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
  • redox-related biomarkers
  • antioxidants
  • heart failure
  • cardiomyopathy
  • toxic cardiomyopathy
  • heart-rhythm-induced cardiomyopathy
  • stress-induced cardiomyopathies
  • peripartum cardiomyopathy
  • inflammatory cardiomyopathy
  • infiltrative cardiomyopathy

Published Papers (2 papers)

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Research

17 pages, 1076 KiB  
Article
Association of NT-proBNP and sST2 with Left Ventricular Ejection Fraction and Oxidative Stress in Patients with Stable Dilated Cardiomyopathy
by Elżbieta Lazar-Poloczek, Ewa Romuk, Wojciech Jacheć, Karolina Wróbel-Nowicka, Agata Świętek and Celina Wojciechowska
Biomedicines 2024, 12(4), 707; https://doi.org/10.3390/biomedicines12040707 - 22 Mar 2024
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Abstract
The aim of this study was to analyze the relationship between levels of sST2, NT-proBNP and oxidative stress markers in patients with reduced ejection fraction (HFrEF) due to non-ischemic cardiomyopathy. A total of 88 patients with HFrEF were divided into four groups based [...] Read more.
The aim of this study was to analyze the relationship between levels of sST2, NT-proBNP and oxidative stress markers in patients with reduced ejection fraction (HFrEF) due to non-ischemic cardiomyopathy. A total of 88 patients with HFrEF were divided into four groups based on left ventricular ejection fraction (≤25% and >25%) and NYHA functional class (group 1—LVEF > 25% and NYHA class I or II; group 2—LVEF > 25% and NYHA class III or IV; group III—LVEF ≤ 25% and NYHA class I or II; group IV—LVEF ≤ 25% and NYHA class III or IV). In 39 (44.32%) patients LVEF was reduced below 25%, and 22 of them (56.41%) were in NYHA functional class III/IV. Of the 49 (55.68%) patients with LVEF ≥ 25%, only 18.37% were in NYHA functional class III/IV (p < 0.001). Patients with LVEF ≥ 25% had lower levels of NT-proBNP, total oxidant status (TOS), total antioxidant capacity (TAC), and oxidative stress index (OSI). The levels of NT-proBNP but not sST-2 correlated positively with NYHA functional class (p < 0.001) and negatively with LVEF (p < 0.001). The levels of sST-2 were associated with increased TAC (p = 0.009) and uric acid (p = 0.040). These findings indicate that only NT-proBNP was related to the severity of heart failure, whereas sST2 correlated with total antioxidant capacity. Therefore, in stable patients with HFrEF due to dilated cardiomyopathy, sST2 may be an additional biomarker reflecting the redox status, but not the severity of heart failure. Full article
(This article belongs to the Special Issue Oxidative Stress Markers in Cardiomyopathy)
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21 pages, 3685 KiB  
Article
7-Hydroxy Frullanolide Ameliorates Isoproterenol-Induced Myocardial Injury through Modification of iNOS and Nrf2 Genes
by Saif Ullah, Taseer Ahmad, Muhammad Ikram, Hafiz Majid Rasheed, Muhammad Ijaz Khan, Taous Khan, Tariq G. Alsahli, Sami I. Alzarea, Musaad Althobaiti and Abdul Jabbar Shah
Biomedicines 2023, 11(9), 2470; https://doi.org/10.3390/biomedicines11092470 - 06 Sep 2023
Viewed by 1065
Abstract
Myocardial infarction (MI) is the principal cause of premature death. Protecting myocardium from ischemia is the main focus of intense research. 7-hydroxy frullanolide (7-HF) is a potent anti-inflammatory agent, showing its efficacy in different acute and chronic inflammatory disorders such as atherosclerosis, suggesting [...] Read more.
Myocardial infarction (MI) is the principal cause of premature death. Protecting myocardium from ischemia is the main focus of intense research. 7-hydroxy frullanolide (7-HF) is a potent anti-inflammatory agent, showing its efficacy in different acute and chronic inflammatory disorders such as atherosclerosis, suggesting it can be a potential cardioprotective agent. For the induction of MI, Sprague–Dawley rats (n = 5) were administered isoproterenol (ISO) 85 mg/kg s.c at 24 h intervals for two days. The potential cardioprotective effect of 7-HF and its mechanisms were explored by in vivo and in vitro methods. 7-HF significantly prevented the extent of myocardial injury by decreasing the infarct size, preserving the histology of myocardial tissue, and reducing the release of cardiac biomarkers. Further, 7-HF increased the mRNA expression of cardioprotective gene Nrf2 and reduced the mRNA expression of iNOS. 7-HF also improved cardiac function by decreasing the cardiac workload through its negative chronotropic and negative ionotropic effect, as well as by reducing peripheral vascular resistance due to the inhibition of voltage-dependent calcium channels and the release of calcium from intracellular calcium stores. In conclusion, 7-HF showed cardioprotective effects in the MI model, which might be due to modulating the expression of iNOS and Nrf2 genes as well as improving cardiac functions. Full article
(This article belongs to the Special Issue Oxidative Stress Markers in Cardiomyopathy)
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