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

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.

Automated summary

Oxidative stress arises from excessive production of ROS and impairment of antioxidant defense systems, leading to damage to cellular biomolecules such as DNA and contributing to cellular damage and disease development. Research has highlighted the significant role of mitochondrial oxidative stress in a variety of pathological processes, from Alzheimer's disease to autoimmune type 1 diabetes, and explored therapeutic approaches targeting oxidative stress.