Role of Mitochondria After Injury

Dear Colleagues,

Mitochondria sustain damage during the course of tissue injury, as seen during severe ischemia in the heart. The targets and mechanisms of mitochondrial injury differ according to the target organ and the disease state. Targets of mitochondrial injury include the electron transport chain, enzymes of intermediary metabolism, mitochondrial membranes, mitochondrial DNA, mitochondrial transporters, the activation of mitochondrial enzyme systems, and the release of mitochondrial proteins. The disease-damaged mitochondria, in turn, may then augment tissue injury, as seen during reperfusion following severe ischemia in the heart. Disease-damaged mitochondria can augment tissue damage via multiple mechanisms, e.g., the production of oxyradicals, impaired energy production, mitochondrial-driven calcium injury, and the activation downstream signaling mechanisms (including those that favor programmed cell death). Damage to mtDNA can limit the repair and recovery of dysfunctional mitochondria. Mitochondrial biogenesis and mitophagy may be impaired. This Special Issue welcomes original research studies, reviews, or opinion papers on the mechanisms and targets of disease-induced mitochondrial damage and/or the role of the damaged mitochondria in augmenting the subsequent tissue injury that impairs organ recovery. Investigations covering potential translational insights are welcomed.

Dr. Edward Lesnefsky
Dr. Qun Chen
Guest Editors

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• electron transport chain
• reactive oxygen signaling
• mitochondrial permeability transition pore
• programmed cell death
• mitochondrial repair
• mitophagy
• energy metabolism