Understanding the mechanisms that prevent acute kidney injury (AKI) progression is key, particularly the role of lipid mediators produced by immune cells called macrophages, which regulate inflammation. Unraveling the function of these lipid mediators is crucial for developing potential therapies (1✔ ✔Trusted Source
MAFB in macrophages regulates PGE2-mediated lipid mediator class switch through ALOX15 in ischemic Acute Kidney Injury
).
Acute kidney injury (AKI) is linked to a poor prognosis, and current treatments are ineffective. However, in this study, researchers focused on the transcription factor MAFB which has been reported to regulate the inflammation-suppressive capacity of macrophages.
They analyzed the function of macrophages in the context of AKI. When AKI was induced in mice specifically lacking MAFB in macrophages (MAFB-deficient mice), the prognosis was worse compared to that of wild-type mice.
Targeting Immune Cells May Hold The Future Treatments
A comprehensive analysis of gene expression in macrophages from the MAFB-deficient mice revealed a marked decrease in the expression of the gene ALOX15; ALOX15 is an enzyme essential for the production of pro-resolving LMs.
Furthermore, the expression of MAFB in macrophages during AKI is regulated by a pro-inflammatory lipid mediator known as PGE2, and MAFB regulates ALOX15 expression under the influence of PGE2. These findings collectively suggest that MAFB plays a critical role in shifting LMs from a pro-inflammatory to a pro-resolving state.
Given that the balance between pro-inflammatory and pro-resolving LMs significantly impacts the prognosis of acute inflammation, the results of this study are expected to contribute to the development of therapeutic and diagnostic methods for AKI and other acute inflammatory diseases.
Reference:
- MAFB in macrophages regulates PGE2-mediated lipid mediator class switch through ALOX15 in ischemic Acute Kidney Injury
– (https://journals.aai.org/jimmunol/article/doi/10.4049/jimmunol.2300844/267125/MAFB-in-Macrophages-Regulates-Prostaglandin-E2)
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