Mitochondrial DNA (mtDNA) mutations result in not only inefficient supply of ATP but also increased production of reactive oxygen species (ROS) such as superoxide anions and hydrogen peroxide in mitochondria of the affected tissues of patients with mitochondrial disease or in elderly subjects. Extensive studies have demonstrated that such an increase of oxidative stress contributes to alterations in the gene expression and activities of enzymes in several metabolic pathways. Several antioxidant enzymes are altered and oxidative damage to DNA, RNA, proteins, and lipids are increased in tissues and cultured cells from mitochondrial disease patients or elderly subjects. The changes at the protein and activity levels of several metabolic pathways result in metabolic reprogramming, which plays an important role in adaptive response and survival of human cells harboring a pathogenic mtDNA mutation. This special issue is focused on the molecular mechanism and consequences of human cell response to pathogenic mtDNA mutation and/or mitochondrial dysfunction.
Prof. Dr. Yau-Huei Wei
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