Mitochondrial Dysfunction and Oxidative Stress in Human Diseases
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".
Deadline for manuscript submissions: 30 November 2025 | Viewed by 19
Special Issue Editor
2. Department of Pediatrics, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA, USA
Interests: mitochondrial disease; bioenergetics; energy metabolism; oxidative stress; respiratory chain; complex I; proton pump; iron-sulfur clusters; quinone; flavin; redox potential; NAD metabolism; GSH
Special Issue Information
Dear Colleagues,
Mitochondria generate more than 90% of the ATP needed by the body to support various cellular activities via oxidative phosphorylation. However, when mitochondria are slightly impaired, some electrons leak from electron transport chains, and directly react with oxygen, causing reactive oxygen species (ROS) to be released. ROS cause damage to various cellular components lipids, DNA, proteins, and other macromolecules, ultimately causing a decline in mitochondrial ATP production and promoting more ROS production. The accumulation of ROS further damages a variety of mitochondrial functions, creating a vicious cycle of oxidative stress and mitochondrial impairment. Mitochondrial dysfunction and oxidative stress have been strongly implicated in the pathogenesis of various human diseases like cancer, neurodegenerative disorders, cardiovascular disease, and metabolic disease. The purpose of this Special Issue is to report on recent progress achieved in this fast-evolving and broad field. We seek submissions of high-quality articles devoted to all aspects of mitochondrial dysfunction and oxidative stress in human diseases including, but not limited to, mitochondrial biology, metabolism, bioenergetics, regulation, signaling, or drug-development and therapeutic strategies targeting mitochondrial dysfunction and oxidative stress to prevent human diseases.
Dr. Eiko Nakamaru-Ogiso
Guest Editor
Manuscript Submission Information
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Keywords
- mitochondrial dysfunction
- oxidative stress
- reactive oxygen species
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