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• W4382361878 abstract "Disulfide bond A oxidoreductase-like protein (DsbA-L) drives acute kidney injury (AKI) by directly upregulating the expression of voltage-dependent anion-selective channels in proximal tubular cells. However, the role of DsbA-L in immune cells remains unclear. In this study, we used an LPS-induced AKI mouse model to assess the hypothesis that DsbA-L deletion attenuates LPS-induced AKI and explore the potential mechanism of DsbA-L action. After 24 hours of LPS exposure, the DsbA-L knockout group exhibited lower serum creatinine levels compared to the WT group. Furthermore, peripheral levels of the inflammatory cytokine IL-6 were decreased. Transcriptomic data analysis revealed a significant down-regulation in the IL-17 and tumor necrosis factor pathways in DsbA-L knockout mice following LPS induction. Metabolomic analysis suggested that arginine metabolism was significantly different between the WT and DsbA-L knockout groups after LPS treatment. Notably, the M1 polarization of macrophages in the kidneys of DsbA-L knockout AKI mice was significantly reduced. Expression of the transcription factors NF-κB and AP-1 was downregulated after DsbA-L knockout. Our results suggest that DsbA-L regulates LPS-mediated oxidative stress, promotes M1 polarization of macrophages, and induces expression of inflammatory factors via the NF-κB/AP-1 pathway." @default.
• W4382361878 created "2023-06-29" @default.
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• W4382361878 date "2023-07-21" @default.
• W4382361878 modified "2023-10-16" @default.
• W4382361878 title "DsbA‐L deletion attenuates LPS‐induced acute kidney injury by modulating macrophage polarization" @default.
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• W4382361878 doi "https://doi.org/10.1002/eji.202250071" @default.
• W4382361878 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/37379419" @default.
• W4382361878 hasPublicationYear "2023" @default.
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