Mitochondrial Dysfunction and Oxidative Damage

Dear Colleagues,

Mitochondrial dysfunction and oxidative stress have been implicated in the pathogenesis of a number of diseases and conditions. The mitochondrial electron transport chain (ETC) is particularly vulnerable to reactive oxygen (ROS) and nitrogen (RNS) species induced impairment either as the result free radical induced damage to the enzyme complexes, mitochondrial DNA or mitochondrial membrane phospholipids. Once impaired the ETC then becomes a major source of ROS generation, which results in further damage to the ETC, as well compounding the cellular oxidative stress. Although the cell possesses a number of antioxidant systems to combat ROS and RNS, during pathological conditions these defences can become overwhelmed resulting in oxidative damage to the biomolecules of the cell and resulting in cellular and consequently, organ dysfunction. Therefore, the use of appropriate antioxidant strategies, especially those that target the mitochondria may be particularly important in the treatment of diseases associated with oxidative stress. Clinical management of oxidative stress and mitochondrial dysfunction is hampered by a lack of consensus on appropriate treatment strategies together with an absence of reliable non-invasive surrogates to monitor disease progression and the treatment response following therapeutic invention

This Special Issue requests original research, mini and full reviews, and perspectives that address the progress and current standing in the field of mitochondrial dysfunction and oxidative stress.

Dr. Iain P. Hargreaves
Guest Editor

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