Oxidative Stress and Mitochondrial Dysfunction in Human Diseases: Pathophysiology, Predictive Biomarkers, Therapeutic

Dear Colleagues,

Mitochondria are important sites for a variety of cellular processes, including amino acid and fatty acid metabolism, the citric acid cycle, nitrogen metabolism, and oxidative phosphorylation to produce ATP. Mitochondria are also an important source of reactive oxygen species (ROS). During the production of ATP, the waste produced by mitochondria is called free radicals. This toxic waste can cause specific changes (mutations) in the genetic material of the mitochondria that damage the mitochondrion itself and can cause cell dysfunction and disease. Mitochondrial disease results when the production of cellular energy is defective. 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 global regulation of gene expression can illuminate the contribution of mitochondria in the development of disease and may lead to the advancement of new and novel therapeutic modalities that exploit mitochondria in treating many maladies. In fact, mitochondrial oxidative stress, commonly associated with aging and age-related pathologies (neurodegenerative syndromes, cardiovascular diseases, endocrine pathologies, diabetes, and cancer), leads to damage to mitochondrial DNA, proteins, and lipids. The increased ROS presence can also induce chronic inflammation, which often characterizes age-related diseases and autoimmune pathologies.

This Special Issue aims to provide a broad and updated overview of the involvement of “Oxidative Stress and Mitochondrial Dysfunction in Human Disease: Pathophysiology, Predictive Biomarkers, Therapeutic” that might shed light on model systems, diagnostic biomarkers, pathophysiological mechanisms, and novel therapeutic approaches. To progress in the knowledge of such intricate issues, contributions by experts in the field in the form of research papers and critical reviews are called for. Potential topics include but are not limited to the following: 1. basic molecular and cellular mechanisms underlying oxidative stress and mitochondrial dysfunction; 2. recent discoveries in animal models to understand the role of oxidative stress in human disorders; 3. new preventive and therapeutic strategies focused on oxidative stress and mitochondrial in human diseases; 4. therapies that act as antioxidants during the repair process l Role of oxidative stress in metabolic diseases.

Dr. Chia-Jung Li
Guest Editor

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