ArticlePloS one2026
Intercellular GAS6-AXL signaling triggers podocyte cuproptosis in acute kidney injury upstream regulated by CEBPD.
Article in PloS one, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
This study aims to investigate the role of cuproptosis, a novel form of regulated cell death, in the transition from acute kidney injury (AKI) to chronic kidney disease (CKD). Multi-omics approaches, including single-cell RNA sequencing (scRNA-seq), spatial transcriptomics, and in vitro experiments based on cells, were integrated to dissect the spatiotemporal regulation of cuproptosis in AKI. Podocytes exhibited the highest cuproptosis activity. A critical intercellular communication axis was identified, wherein endothelial cell-derived GAS6 signals through the podocyte receptors AXL/TYRO3. The transcription factor CEBPD was upregulated early in AKI and was found to positively regulate the GAS6-related pathway, with its target genes enriched in TGF-β and JAK-STAT signaling, ultimately leading to receptor activation and cuproptosis. Spatially, CEBPD activation preceded the increase in AXL, followed by late-phase upregulation of GAS6. The alteration in AXL protein expression was confirmed in vitro.Our study reveals a CEBPD-mediated transcriptional program that drives podocyte cuproptosis by transactivating the AXL receptor, providing novel mechanistic insights into the AKI-to-CKD transition.
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