Mitochondria-Mediated Oxidative Stress in Diseases: Cell Death and Treatment

Dear Colleagues,

Mitochondria are essential organelles with versatile functions in cellular metabolism. Apart from their best-known function as main producers of energy, they are fully integrated into the cellular metabolism, being crucial for proliferation, cell signal transmission and adaptation to external stressors, in addition to maintaining calcium and redox homeostasis and regulating apoptosis. Mitochondria are the principal organelles responsible for reactive oxygen species (ROS) generation in the cell, with the respiratory chain being a major ROS producer. ROS play a dual role in biological systems. They serve as essential mediators in cell signaling, modifying ion channels and transporters, kinases and the proteasome system and regulating division, development, differentiation, systemic responses, adaptation to stress, interactions with other organisms and cell death. Mild redox stresses can protect an organism from subsequent, more severe stresses and improve metabolism and the immune system, thus prolonging an individual’s lifespan. To highlight positive effects of ROS on cells, the term “oxidative eustress” was introduced as an extension of the initial definition of “oxidative stress”, in contrast to “oxidative distress”, referring to excessive production of ROS, which is largely derived from mitochondrial dysfunction or an imbalance between ROS generation and clearance. Mitochondria-mediated oxidative distress often causes multifarious impairment to cells, thereby leading to the aggravation of many diseases and apoptosis induction. Muscle atrophy and frailty, cardiac disorders, age-related chronic wounds, obesity-related type 2 diabetes, the aging of mtDNA mutator mice, neurodegenerative disorders (Alzheimer’s, Parkinson’s and Huntington’s diseases) and atrophy of thymus epithelial cells are the most likely impacts of mitochondrial ROS (mROS). In cancer cells, mROS production contributes to evolution toward more aggressive phenotypes. Moreover, findings have emerged implicating a fundamental role of mROS in even highly glycolytic cells with relatively low energy requirements and mitochondrial content such as stem cells, epithelia and neutrophils. Fortunately, the most effective mitochondria-targeted (mitochondria-addressed) cationic lipophilic antioxidants are able to ameliorate or even prevent pathologies, contributing to a novel field of study, named “mitotherapy”.

Topics of interest for this Special Issue include the following:

1. The role of mitochondrial oxidative stress in the pathogenesis of various diseases, including neurodegenerative diseases, cardiovascular diseases, cancer and aging-related diseases.
2. Therapeutic approaches targeting mitochondrial oxidative stress for the treatment of these diseases, such as mitochondria-targeted antioxidants, mitophagy inducers and mitochondrial biogenesis enhancers.
3. The role of mitochondrial dynamics and mitochondrial DNA damage in the development and progression of diseases associated with mitochondrial oxidative stress.
4. The interplay between mitochondrial oxidative stress and other cellular pathways, such as inflammation, autophagy and immune response in the pathogenesis of various diseases.
5. The identification and validation of novel biomarkers of mitochondrial oxidative stress in the diagnosis, prognosis and therapeutic monitoring of diseases.

This Special Issue, entitled “Mitochondria-Mediated Oxidative Stress in Diseases: Cell Death and Treatment”, aims to highlight and promote the latest scientific achievements in this exciting field, presenting original and update-to-date contributions.

Prof. Dr. Renata A. Zvyagilskaya
Guest Editor

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• mitochondrial dysfunction
• reactive oxygen species
• oxidative stress
• mitochondrial biogenesis
• mitotherapy
• neurodegenerative diseases
• cardiovascular diseases
• cancer
• biomarkers
• mitochondrial dynamics