Fig. 8: Working model. | Communications Biology

Fig. 8: Working model.

From: Macrophage-derived exosomal aminopeptidase N aggravates sepsis-induced acute lung injury by regulating necroptosis of lung epithelial cell

Fig. 8

Our data demonstrated that c-Myc directly induces APN/CD13 expression in LPS-stimulated macrophages, which promotes APN/CD13 secretion into exosomes. In addition, we found that exosomal APN/CD13 from macrophages regulates the necroptosis of epithelial cells by binding to the cell surface receptor TLR4, enhancing NF-κB activity and mitochondrial dysfunction, and promoting RIPK1/RIPK3 necroptosis. In conclusion, our findings reveal that the communication between macrophages and lung epithelial cells via exosomal APN/CD13 leads to mitochondrial dysfunction, augments inflammation and increases cell apoptosis, so that participates in the occurrence of sepsis-induced ALI.

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