What is it about?
This paper focused on the pathogenesis of endothelial injury in sepsis-induced AKI. AND we have shown for the first time that inhibition of PI3Kγ alleviated endothelial cell injury in the kidneys, preserved endothelial cell function and repaired endothelial cell injury via the Akt signaling pathway, indicating that PI3Kγ/Akt signaling is pivotal for regulating endothelial cell function in AKI in response to sepsis.
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Why is it important?
Our findings show that the pathogenesis of endothelial injury in sepsis-induced AKI can not be ignored, and the PI3Kγ/Akt signaling is pivotal for regulating endothelial cell function in AKI in response to sepsis. It will provide direction for exploring therapeutic targets and strategies in sepsis-induced AKI.
Perspectives
We have spent a lot of time and effort in this study, and found that sepsis organ dysfunction is still a difficult problem, and there are still many problems that need to be clarified and solved. In the future, we will continue to devote ourselves to the research in sub-fields to be more detailed.
Han Li
Read the Original
This page is a summary of: Inhibition of Phosphoinositide 3-Kinase Gamma protects endothelial cells via the Akt signaling pathway in sepsis-induced acute kidney injury, Kidney and Blood Pressure Research, September 2022, Karger Publishers,
DOI: 10.1159/000526916.
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Contributors
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