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Inflammatory cells play a role in the pathogenesis of renal ischemia-reperfusion injury. In response to an ischemia-reperfusion injury, we investigated the effects of phosphoinositide 3 kinase u03b3 in the kidney. Compared to wild-type mice, PI3Ku03b3 knockout mice had less IRI in the kidney, and there were fewer tubular apoptotic cells in the kidney. These results show that PI3Ku03b3 plays a crucial role in kidney injury in IRI, suggesting that PI3Ku03b3 inhibition may be a potential therapeutic technique for the prevention of ischemia-reperfusion-induced kidney injury.
Source link: https://doi.org/10.3390/cells11050772
In critically ill patients, acute kidney injury plays a significant role in morbidity and mortality. AKI is also a risk factor for chronic kidney disease progression and progression. In AKI, a comprehensive, mechanistic analysis of mitochondrial function and renal metabolism could lead to the development of novel therapies. For the treatment of AKI, we also outline current therapeutic protocols that focus on mitochondrial function and metabolic pathways.
Source link: https://doi.org/10.3390/jcm10173991
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