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Demonstrates the SPP1-CD44 axis regulates inflammation in acute kidney injury, suggesting new therapeutic targets.
functional experiments further confirmed that blocking the SPP1-CD44 axis, using siRNA, neutralizing antibodies, or conditional knockout strategies, effectively alleviates renal IRI in mice, reduces macrophage infiltration, and diminishes the inflammatory response. Overall, this study delineates a novel mechanism in which injured tubular cell-derived SPP1 communicates with macrophage CD44 to regulate immunometabolism and inflammatory polarization via the PI3K/AKT-PKM2 signaling module at the single-cell and metabolic levels. These findings provide both a potential therapeutic target and a mechanistic framework for the prevention and treatment of AKI.
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Gong et al. (2026) studied this question.
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