Special Issue "Mitochondrial Function in Human Health and Disease"
Deadline for manuscript submissions: 31 December 2023 | Viewed by 13612
Mitochondria play critical metabolic roles in fatty acid oxidation, the Krebs cycle, and oxidative phosphorylation. All of these metabolic processes result in reactive oxygen species (ROS) production. ROS is toxic to cells because it causes oxidative damage to mitochondrial lipids, DNA, and proteins. Damaged mitochondria also release high levels of Ca2+ and cytochrome C to induce apoptosis. To control the quality and quantity of mitochondria, selective autophagy, known as mitophagy, plays an important role by eliminating damaged mitochondria. Besides causing ROS damage in mitochondria, alterations in mitochondrial function through mutations in either the mitochondrial or nuclear genome have also been found to be associated with various diseases, such as cancer, aging, metabolic disorders, etc. The first known involvement of mitochondria in cancer came from Warburg’s landmark observation that tumors produce excess lactate in the presence of oxygen, now known as the “Warburg effect”, which is a form of aerobic glycolysis. Activation of cellular signaling transduction pathways, such as the PI3’K/PTEN/Akt pathway, also plays an important role in shifting metabolism from oxidative to glycolytic phosphorylation. Now, more evidence suggests that AKT kinase activity in mitochondria is crucial for cellular defense to extrinsic insults such as ischemia reperfusion. This special issue elucidates various aspects of mitochondrial function in cancer, kidney disease, apoptosis, and autophagy, and further discusses the therapeutic potential of targeting mitochondria.
Dr. Yumay Chen
Manuscript Submission Information
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- mitochondial genesis and disease
- mitochondrial function and aging
- mitochondrial dysfunction and cancer
- mitochondrial function and apoptosis
- mitochondrial AKT