AI Article Synopsis
- Oxidative stress occurs when there's an overproduction of reactive oxygen species (ROS) and a failure of antioxidant defenses, primarily due to mitochondrial respiration.
- ROS can cause significant damage to cellular components, including DNA, leading to mitochondrial dysfunction, cell damage, and diseases like Alzheimer’s and type 1 diabetes.
- The review highlights recent research on the link between mitochondrial oxidative stress and various diseases, as well as exploring potential therapeutic strategies to manage oxidative stress.
Article Abstract
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.
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|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8707347 | PMC |
| http://dx.doi.org/10.3390/ijms222413384 | DOI Listing |
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