Oxidative Stress and Mitochondrial Dysfunction in Human Diseases
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".
Deadline for manuscript submissions: 20 September 2026 | Viewed by 377
Editor
Special Issue Information
Dear Colleagues,
Mitochondria reside at the crossroads of catabolic and anabolic metabolism—the essence of life. Mitochondria play a key role in various cellular processes, including amino acid and fatty acid metabolism, the citric acid cycle, nitrogen metabolism, and oxidative phosphorylation, which produces ATP. The waste produced by mitochondria during the production of ATP is indeed formalized in terms of free radical production. The phenomenon of ROS-induced ROS release (RIRR) was highlighted in pioneering work, which showed that mitochondrial generation of reactive oxygen species (ROS) can trigger further ROS bursts in a feed-forward manner. As a result, ROS homeostasis and oxidative stress have become major areas of research. This toxic waste can cause specific changes (including mutations) in the genetic material of the mitochondria that damage the mitochondrion itself and can cause cell dysfunction and disease.
Current research continues to elucidate how the mitochondrial structure and function adapt in response to the tissue-specific requirements of energy, growth, repair and renewal. Mitochondria respond to intrinsic and extrinsic stresses, altering cell and organismal function by inducing metabolic signaling within and between cells and tissues.
Because of the omnipresence of ROS in cells and contribution of mitochondria in the production and removal of cellular ROS, a greater understanding of oxidative stress in mitochondria, under both normal and disease-causing conditions, and the involvement of mitochondrial ROS in the global regulation of gene expression can further explain the contribution of mitochondria to the development of disease and may lead to the advancement of new and novel therapeutic modalities that exploit mitochondria in treating different maladies.
In this Special Issue, we explore the importance of mitochondrial functions and oxygen stress for health, aging, and a wide range of diseases. We are also aware that molecules capable of positively modulating cellular metabolism by improving mitochondrial bioenergetics and energy metabolism, while inhibiting the production of oxidative stress, are expected to exert beneficial protective effects.
Mitochondrial dysfunction and oxidative stress play a significant role in aging, cancer, and age-related neurodegenerative and metabolic syndromes. Mitochondria are also involved in the inflammatory response associated with neurological disorders such as Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, and epilepsy.
Therefore, we invite submissions of research on any pathology showing a clear link with oxidative stress and mitochondria.
Dr. Patrice X. Petit
Guest Editor
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Keywords
- aging
- DAMPs
- inflammation
- Fenton reaction
- ferroptosis
- hydroperoxide
- mitochondria
- mitophagy
- NIX
- NLRP3
- oxidized mtDNA
- RIRR
- superoxide anions
- stem cells
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