Akt activation improves oxidative phosphorylation in renal proximal tubular cells following nephrotoxicant injury

摘要

stress stimuli, including ischemia, hypoxia, drugs, and toxicants, induce mitochondrial injury in a variety of cell types (2, 18). Mitochondrial dysfunction and the resulting energy deficits are common mechanisms of cell death (16, 22, 30, 31). Cells that require high energy input and are dependent on oxidative phosphorylation for ATP production, such as cardiac myocytes and renal cortical tubules, are particularly susceptible to injury and death caused by inhibition of mitochondrial energy metabolism (16, 18, 30).