Mitochondrial energetics in the kidney
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Cites background from "Mitochondrial energetics in the kid..."
...Although excessive mtROS have been shown to disturb multiple pathways involved in calcium homeostasis, mitochondrial permeability, and cytochrome C release and to directly induce renal cell death [3,38,39], their specific roles in mitochondrial damage and inflammation during IRI-AKI are not completely understood....
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...upon reperfusion, leading to a series of events that follow IRI-induced AKI (IRI-AKI) and include mitochondrial damage, energy depletion, tubular apoptosis and necrosis [3-5]....
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...Increasing evidence indicates that the mitochondrion is a main source of intracellular ROS, and ~90% of ROS are generated in mitochondria [3]....
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...The overproduction of reactive oxygen species (ROS) contributes to multiple cellular processes related to renal injury, such as cytosolic calcium overload, energy depletion, apoptosis/necrosis, and inflammation [3]....
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