GEO series
DsbA-L deficiency attenuates LPS-induced acute kidney injury via NF-κB/AP-1 regulation of macrophage polarization
GSE202753
Mus musculus
Expression profiling by high throughput sequencing
13 samples
2025/05/10
GPL24247
Summary
Background: Disulfide bond A oxidoreductase-like protein (DsbA-L) drives acute kidney injury (AKI) progression in proximal tubular cells by directly upregulating voltage-dependent anion-selective channel levels; however, its role in immune cells remains unclear. Methods: We used the mouse model of AKI induced by LPS to explore the mechanism of how DsbA-L deficiency regulating macrophages and kidney injury under the guidance of transcriptome and metabolic. Results: DsbA-L knockout resulted in significant changes in the JNK pathway, which might affect macrophage polarization to reduced AKI injury based on the cellular and stimulus-dependent characteristics of JNK function
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