Special Issues
Table of Content

Mitochondrial Dysfunction in Metabolic and Neuromuscular Diseases: Mechanisms and Therapeutic Strategies

Submission Deadline: 10 May 2025 View: 266 Submit to Special Issue

Guest Editors

Dr. Mikhail V. Dubinin

Email: dubinin1989@gmail.com 

Affiliation: Department of Biochemistry, Cell Biology and Microbiology, Mari State University, pl. Lenina 1, Yoshkar-Ola 424001, Russia

Homepage: 

Research Interests: muscles, ion homeostasis, calcium, myopathy, diabetes, oxidative stress, mitochondria

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Prof. Dr. Konstantin N. Belosludtsev

Email: bekonik@gmail.com

Affiliation: Laboratory of Mitochondrial Transport, Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences, Institutskaya 3, 142290 Pushchino, Russia

Homepage:

Research Interests: mitochondria, biophysics, diabetes mellitus, myopathy, mitochondrial Ca2+ transport, reactive oxygen species, lipids

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Summary

Mitochondria play a crucial role in the pathogenesis of a wide range of diseases, from metabolic disorders to neuromuscular conditions. This special issue aims to delve into the complex mechanisms by which mitochondrial dysfunction contributes to these diseases, with a particular focus on diabetes, muscular dystrophies, and neurodegenerative pathologies.

 

By bringing together groundbreaking research from leading experts, this issue seeks to illuminate novel pathways and therapeutic approaches that target mitochondrial function. Key areas of focus include but are not limited to:

1. Mitochondria in Metabolic Disorders:

   - Investigating how mitochondrial dysfunction drives insulin resistance and β-cell failure in diabetes.

   - Understanding the role of mitochondrial energy metabolism in the development and complications of metabolic diseases.

2. Mitochondrial Dysfunction in Neuromuscular Diseases:

   - Exploring the structural and functional changes in mitochondria in congenital and acquired muscular dystrophies and cardiomyopathies.

   - Evaluating potential therapies aimed at restoring mitochondrial function in these conditions.

3. Oxidative Stress and ROS in Disease Progression:

   - Assessing the impact of mitochondrial-generated reactive oxygen species (ROS) on cellular damage and disease progression.

   - Investigating antioxidant strategies to mitigate oxidative stress in metabolic and neuromuscular diseases.

4. Calcium Signaling and Mitochondrial Dysregulation:

   - Examining the role of calcium homeostasis in mitochondrial dysfunction, particularly in muscle and cardiac tissues.

   - Identifying potential therapeutic targets within calcium signaling pathways to improve mitochondrial health.

5. Energy Metabolism and Disease Development:

   - Uncovering how disruptions in mitochondrial energy production contribute to the pathogenesis of both common and rare diseases.

   - Highlighting novel metabolic interventions to correct mitochondrial dysfunction.

6. Innovative Therapeutic Approaches Targeting Mitochondria:

   - Developing gene therapies, pharmacological treatments, and mitochondrial transplantation strategies to enhance mitochondrial function.

   - Exploring new approaches to modulate mitochondrial activity and improve disease outcomes.

 

Through this special issue, we aim to foster interdisciplinary research and advance our understanding of mitochondrial involvement in various diseases. We welcome original research articles, comprehensive reviews, and perspectives that investigate the multifaceted roles of mitochondria in disease mechanisms and therapeutic innovation. By showcasing the latest discoveries and addressing the challenges in the field, this issue aspires to pave the way for novel treatments and improved patient outcomes.


Keywords

mitochondria, metabolic disorders, neuromuscular diseases, diabetes, muscular dystrophies, cardiomyopathies, oxidative stress, ROS, calcium signaling, energy metabolism, therapeutic strategies

Published Papers


  • Open Access

    ARTICLE

    20-Hydroxyecdysone Partially Alleviates Ischemia/Reperfusion-Induced Damage of Mouse Hind Limb Skeletal Muscle

    Alena A. Semenova, Anastasia D. Igoshkina, Alena A. Cherepanova, Natalia V. Mikina, Anastasia E. Stepanova, Olga E. Krasnoshchekova, Vyacheslav A. Sharapov, Rimma G. Savchenko, Lyudmila V. Parfenova, Mikhail V. Dubinin
    BIOCELL, DOI:10.32604/biocell.2025.061798
    (This article belongs to the Special Issue: Mitochondrial Dysfunction in Metabolic and Neuromuscular Diseases: Mechanisms and Therapeutic Strategies)
    Abstract Objectives: Skeletal muscle ischemia/reperfusion injury (IRI) occurs as a result of a marked reduction in arterial perfusion to a limb and can lead to tissue death and threaten limb viability. TTis work assessed the effects of 20-hydroxyecdysone (20E) on hindlimb skeletal tissue following tourniquet-induced ischemia/reperfusion injury. Methods: Animals were divided into 4 groups—control group (Control), Control + 20E (C + 20E), mice with IRI (IRI), and mice with IRI + 20E (IRI + 20E). IRIwas modeled by applying a tourniquet to the hind limb for 2 hwith reperfusion for 1 h. 5 mg/kg of 20E was… More >

  • Open Access

    ARTICLE

    Protective Effects of Probiotics against Methotrexate-Induced Intestinal Toxicity in the Mice Model

    KSENIA S. STAFEEVA, NATALIA A. SAMOYLOVA, OLGA A. KARANDEEVA, VERONIKA V. NESTEROVA, KIRILL A. STARODUBTSEV, EVGENY V. MIKHAILOV, ILYA O. KRUTOV, EVGENY S. POPOV, NATALIA S. RODIONOVA, ANASTASIA V. KOKINA, ARTEM P. GUREEV
    BIOCELL, Vol.49, No.1, pp. 7-20, 2025, DOI:10.32604/biocell.2024.058339
    (This article belongs to the Special Issue: Mitochondrial Dysfunction in Metabolic and Neuromuscular Diseases: Mechanisms and Therapeutic Strategies)
    Abstract Objective: The objective of this study was to determine the level of methotrexate (MTX) toxicity in the intestines of mice and to evaluate the protective effect of probiotics composed of Streptococcus, Bifidobacterium, and Lactobacillus species on intestinal cells during MTX treatment. Methods: Mice were divided into three groups: control, MTX group (received MTX injections), and MTX + probiotics group (received MTX injections along with a diet containing probiotics). Morphological and histological changes, the level of mitochondrial DNA (mtDNA) damage, the level of lipid peroxidation products, and gene expression in the mice’s small intestine were assessed. Results: We… More >

    Graphic Abstract

    Protective Effects of Probiotics against Methotrexate-Induced Intestinal Toxicity in the Mice Model

  • Open Access

    ARTICLE

    MKT-077 normalizes mitochondrial function and mitigates cardiac pathology in mdx mice

    MIKHAIL V. DUBININ, IRINA B. MIKHEEVA, ANASTASIA E. STEPANOVA, NATALIA V. MIKINA, DANIIL V. SUSHENTSOV, VYACHESLAV A. SHARAPOV, ALENA A. CHEREPANOVA, VALENTIN V. LOSKUTOV, KONSTANTIN N. BELOSLUDTSEV
    BIOCELL, Vol.48, No.12, pp. 1815-1825, 2024, DOI:10.32604/biocell.2024.058068
    (This article belongs to the Special Issue: Mitochondrial Dysfunction in Metabolic and Neuromuscular Diseases: Mechanisms and Therapeutic Strategies)
    Abstract Objectives: Duchenne muscular dystrophy (DMD) is characterized by the development of cardiac pathology secondarily expressed in mitochondrial dysfunction. DMD treatment includes support for mitochondrial function. The purpose of this work was to evaluate the effects of the lipophilic cation MKT-077, capable of modulating mitochondrial activity, on the structure and function of cardiac mitochondria in mdx and wild-type mice, as well as the state of this organ. Methods: Animals were divided into 4 groups: wild type (WT), WT + 5 mg/kg MKT-077, mdx, mdx + 5 mg/kg MKT-077. MKT-077 was administered intraperitoneally daily for 28 days. Finally, we… More >

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