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12.4
6.6
Journals
Antioxidants
Special Issues
Oxidative Stress in Striated Muscle and Other Tissues
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Oxidative Stress in Striated Muscle and Other Tissues

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 (30 June 2025) | Viewed by 2034

Special Issue Editor

Prof. Dr. Enrique Jaimovich

E-Mail Website
Guest Editor
Muscle Physiology Laboratory, Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Santiago 8380000, Chile
Interests: skeletal muscle physiology; excitation–transcription coupling; gene expression; muscle metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

ROS play an important signaling role in skeletal and cardiac muscles, as well as in other tissues closely associated with calcium signals that may be or may be not involved in muscle contraction. Several signaling pathways in striated muscle can be activated by an increase in reactive oxygen species (ROS) and reactive nitrogen species (RNS) production. The large magnitude of calcium signals involved in both the contractile process and the deleterious processes induced by excess ROS/RNS production has made the study of the physiological role of ROS difficult and has restricted our in-depth research of these events for many years. Abnormal ROS/RNS production appears to be involved in several striated muscle-related diseases, including muscle wasting, muscular dystrophies, aging-related sarcopenia, cardiac wasting and cancer cachexia. Metabolic diseases such as obesity are also related to abnormal ROS/RNS handling by muscle cells, leading to insulin resistance and T2D.

We invite you to submit your latest research findings or a review article to this Special Issue, which will collate current research in both striated muscle and exercise concerning ROS/RNS production, ROS/RNS regulation and ROS-/RNS-related deleterious processes and diseases. Collating this new knowledge of ROS/RNS homeostasis in striated muscle will provide important insights into the fine-tuning and physiological impact of important signaling within muscle cells.

Prof. Dr. Enrique Jaimovich
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

  • ROS/RNS production
  • mitochondria ROS
  • NADPH oxidase
  • metabolic regulation
  • cardiac oxidative stress
  • ROS sources
  • exercise-induced ROS/RNS
  • antioxidants
  • ROS/RNS in disease

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Published Papers (2 papers)

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Research

17 pages, 1850 KB  
Article
Impact of SGLT2i on Cardiac Remodeling and the Soleus Muscle of Infarcted Rats
by Lidiane Moreira Souza, Felipe Cesar Damatto, Bruna Brasil Brandão, Eder Anderson Rodrigues, Anna Clara Consorti Santos, Rafael Campos França Silva, Mariana Gatto, Luana Urbano Pagan, Paula Felippe Martinez, Gilson Masahiro Murata, Leonardo Antonio Mamede Zornoff, Paula Schmidt Azevedo Gaiolla, Inês Falcão-Pires, Katashi Okoshi and Marina Politi Okoshi
Antioxidants 2025, 14(6), 647; https://doi.org/10.3390/antiox14060647 - 28 May 2025
Cited by 1 | Viewed by 710
Abstract
Skeletal muscle changes occur in heart failure (HF). Despite the cardioprotective effects of sodium–glucose co-transporter 2 (SGLT2) inhibitors in HF, their impact on skeletal muscle remains poorly understood. We investigated the effects of the SGLT2 inhibitor empagliflozin (EMPA) on cardiac remodeling and the [...] Read more.
Skeletal muscle changes occur in heart failure (HF). Despite the cardioprotective effects of sodium–glucose co-transporter 2 (SGLT2) inhibitors in HF, their impact on skeletal muscle remains poorly understood. We investigated the effects of the SGLT2 inhibitor empagliflozin (EMPA) on cardiac remodeling and the soleus muscle of rats with myocardial infarction (MI)-induced HF. Methods: One week after MI induction, rats were assigned to Sham, Sham + EMPA, MI, and MI + EMPA groups. EMPA was administered (5 mg/kg/day) for 12 weeks. Results: MI + EMPA and MI had dilated left cardiac chambers; the left atrium diameter and left ventricle end-diastolic area were smaller in MI + EMPA than MI. The ejection fraction did not differ between infarcted groups. MI + EMPA had a larger soleus cross-sectional area and higher Type II myosin heavy chain expression than MI. Carbonylated protein and malondialdehyde levels were lower and superoxide dismutase activity higher in MI + EMPA than MI. Respiratory Complex I expression was higher in MI + EMPA than MI. Metabolic enzyme activities, altered in MI, were normalized in MI + EMPA. EMPA up-regulated anabolic proteins and down-regulated catabolic proteins. Conclusion: Empagliflozin attenuates infarction-induced cardiac remodeling in rats. In soleus muscle, empagliflozin preserves cell trophism, reduces oxidative stress, normalizes muscle and mitochondrial metabolism, and positively modulates proteins involved in synthesis and degradation-related pathways. Full article
(This article belongs to the Special Issue Oxidative Stress in Striated Muscle and Other Tissues)
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19 pages, 8581 KB  
Article
Growth-Associated Protein-43 Loss Promotes Ca2+ and ROS Imbalance in Cardiomyocytes
by Michele Bevere, Caterina Morabito, Delia Verucci, Noemi Di Sinno, Maria A. Mariggiò and Simone Guarnieri
Antioxidants 2025, 14(3), 361; https://doi.org/10.3390/antiox14030361 - 19 Mar 2025
Viewed by 753
Abstract
Growth-Associated Protein-43 (GAP-43) is a calmodulin-binding protein, originally found in neurons, that in skeletal muscle regulates the handling of intracellular Ca2+ dynamics. According to its role in Ca2+ regulation, myotubes from GAP-43 knockout (GAP-43−/−) mice display alterations in spontaneous [...] Read more.
Growth-Associated Protein-43 (GAP-43) is a calmodulin-binding protein, originally found in neurons, that in skeletal muscle regulates the handling of intracellular Ca2+ dynamics. According to its role in Ca2+ regulation, myotubes from GAP-43 knockout (GAP-43−/−) mice display alterations in spontaneous Ca2+ oscillations and increased Ca2+ release. The emerging hypothesis is that GAP-43 regulates CaM interactions with RyR and DHPR Ca2+ channels. The loss of GAP-43 promotes cardiac hypertrophy in newborn GAP-43−/− mice, extending the physiological role of GAP-43 in cardiac muscle. We investigated the role of GAP-43 in cardiomyocytes derived from the hearts of GAP-43−/− mice, evaluating intracellular Ca2+ variations and the correlation with the levels of reactive oxygen species (ROS), considering their importance in cardiovascular physiology. In GAP-43−/− cardiomyocytes, we found the increased expression of markers of cardiac hypertrophy, Ca2+ alterations, and high mitochondria ROS levels (O2•−) together with increased oxidized functional proteins. Treatment with a CaM inhibitor (W7) restored Ca2+ and ROS alterations, possibly due to high mitochondrial Ca2+ entry by a mitochondrial Ca2+ uniporter. Indeed, Ru360 was able to abolish O2•− mitochondrial production. Our results suggest that GAP-43 has a key role in the regulation of Ca2+ and ROS homeostasis, alterations to which could trigger heart disease. Full article
(This article belongs to the Special Issue Oxidative Stress in Striated Muscle and Other Tissues)
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