Mitochondrial Oxidative Stress-A Causative Factor and Therapeutic Target in Many Diseases

• Published in: International journal of molecular sciences 2021-12, Vol.22 (24), p.13384
• Main Authors: Kowalczyk, Paweł, Sulejczak, Dorota, Kleczkowska, Patrycja, Bukowska-Ośko, Iwona, Kucia, Marzena, Popiel, Marta, Wietrak, Ewa, Kramkowski, Karol, Wrzosek, Karol, Kaczyńska, Katarzyna
• Format: Article
• Language: English
• Subjects: Adenosine triphosphate; Alzheimer's disease; Animals; antioxidant therapy; Antioxidants; Antioxidants - pharmacology; Apoptosis; Biomolecules; Cell division; Cytochrome; Diabetes mellitus (insulin dependent); Disease; Disease - etiology; Enzymes; Free radicals; Free Radicals - metabolism; Genes; Genomes; Humans; Lipids; Metabolism; Mitochondria; Mitochondria - metabolism; mitochondrial diseases; Mitochondrial Diseases - physiopathology; Mitochondrial DNA; Mutation; Oxidation; Oxidative stress; Oxidative Stress - physiology; Phosphorylation; Physiology; Proteins; Reactive oxygen species; Reactive Oxygen Species - adverse effects; Reactive Oxygen Species - metabolism; Respiration; Review; Therapeutic targets
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms222413384

The excessive formation of reactive oxygen species (ROS) and impairment of defensive antioxidant systems leads to a condition known as oxidative stress. The main source of free radicals responsible for oxidative stress is mitochondrial respiration. The deleterious effects of ROS on cellular biomolecules, including DNA, is a well-known phenomenon that can disrupt mitochondrial function and contribute to cellular damage and death, and the subsequent development of various disease processes. In this review, we summarize the most important findings that implicated mitochondrial oxidative stress in a wide variety of pathologies from Alzheimer disease (AD) to autoimmune type 1 diabetes. This review also discusses attempts to affect oxidative stress as a therapeutic avenue.