Special Issues
Table of Content

MitoROS: Exploring Mitochondria and Oxidative Stress

Submission Deadline: 31 May 2026 View: 1515 Submit to Special Issue

Guest Editors

Prof. Dr. Mikhail V. Dubinin

Email: dubinin1989@gmail.com

Affiliation: Department of Biochemistry, Cell Biology and Microbiology, Mari State University, 424001, Yoshkar-Ola, 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: Mari State University

Homepage:

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

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Summary

We are pleased to announce a special issue of BIOCELL entitled «MitoROS: Exploring Mitochondria and Oxidative Stress», focusing on mitochondrial biology, oxidative stress, and their role in human disease pathogenesis. This issue is inspired by the Young Scientists' School «MitoROS: Study of Mitochondria and Oxidative Stress» (September 12-14, 2025, Yoshkar-Ola, Russia, Mari State University), and we are delighted to share these materials with researchers working in these fields.

Scope of the Special Issue
This issue will cover cutting-edge research and reviews on:
· Mitochondrial dysfunction in disease pathogenesis with an emphasis on mechanisms elucidated at the cellular or subcellular level
· Oxidative stress and redox signaling focusing on their effects on cell signaling and cellular functions
· Advances in structural mitochondriology accompanied by functional and mechanistic insights at the cell level
· Gene and cell therapy approaches for mitochondrial disorders validated in cell-based models to demonstrate underlying cellular mechanisms
· Innovative techniques in mitochondrial research that enable mechanistic studies in cells or subcellular systems


Submission Guidelines
We invite original research articles, reviews, and short communications from scientists worldwide. Manuscripts should clearly include cellular or subcellular experiments that uncover mechanisms, not solely descriptive or animal-level observations, in line with BIOCELL standards.

Submission deadline: 31 December 2025

Why Submit?
· High visibility in a thematically focused issue
· Contributions from leading experts in the field
· Opportunity to share your work with a broad scientific audience and to present mechanistic insights at the cellular level that advance understanding of mitochondria and oxidative stress in disease.


Graphic Abstract

MitoROS: Exploring Mitochondria and Oxidative Stress

Keywords

mitochondria, oxidative stress, mitochondrial dysfunction, reactive oxygen species (ROS), mitochondrial diseases, redox signaling, cell therapy, gene therapy, flow cytometry, sequencing, biomedicine, mitochondrial biogenesis, mitochondrial medicine, metabolic disorders, neurodegeneration

Published Papers


  • Open Access

    ARTICLE

    Cellular Knockdown of SELENOM Promotes Apoptosis Induction in Human Glioblastoma (A-172) Cells via Redox Imbalance

    Egor A. Turovsky, Elena G. Varlamova
    BIOCELL, DOI:10.32604/biocell.2025.073728
    (This article belongs to the Special Issue: MitoROS: Exploring Mitochondria and Oxidative Stress)
    Abstract Objectives: Glioblastoma multiforme (GBM) is highly resistant to apoptosis. This study investigates the role of Selenoprotein M (SELENOM), a redox-regulating protein, in the response of human glioblastoma A-172 cells to staurosporine (STS) and hyperthermia. Methods: A stable SELENOM-knockdown (SELENOM-KD) cell line was created. We measured reactive oxygen species (ROS), mitochondrial membrane potential (ΔΨm), cell death, and apoptotic gene expression. Results: SELENOM-KD increased basal ROS levels and induced mitochondrial dysfunction. It sensitized cells to STS-induced apoptosis, enhancing the upregulation of pro-apoptotic genes. Conversely, under hyperthermia (42°C), SELENOM-KD cells exhibited significant thermoresistance, with 52% survival vs. 99% death More >

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