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• W2098070914 abstract "Retinoic acid (RA) has been used therapeutically to reduce injury and fibrosis in models of AKI, but little is known about the regulation of this pathway and what role it has in regulating injury and repair after AKI. In these studies, we show that RA signaling is activated in mouse and zebrafish models of AKI, and that these responses limit the extent of injury and promote normal repair. These effects were mediated through a novel mechanism by which RA signaling coordinated the dynamic equilibrium of inflammatory M1 spectrum versus alternatively activated M2 spectrum macrophages. Our data suggest that locally synthesized RA represses proinflammatory macrophages, thereby reducing macrophage-dependent injury post-AKI, and activates RA signaling in injured tubular epithelium, which in turn promotes alternatively activated M2 spectrum macrophages. Because RA signaling has an essential role in kidney development but is repressed in the adult, these findings provide evidence of an embryonic signaling pathway that is reactivated after AKI and involved in reducing injury and enhancing repair." @default.
• W2098070914 created "2016-06-24" @default.
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• W2098070914 date "2016-02-01" @default.
• W2098070914 modified "2023-09-26" @default.
• W2098070914 title "Retinoic Acid Signaling Coordinates Macrophage-Dependent Injury and Repair after AKI" @default.
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• W2098070914 doi "https://doi.org/10.1681/asn.2014111108" @default.
• W2098070914 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4731115" @default.
• W2098070914 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/26109319" @default.
• W2098070914 hasPublicationYear "2016" @default.
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