Nicotinamide mononucleotide protects against diabetic nephropathy <i>via</i> IL-6/Rab5-mediated crosstalk between proximal tubular epithelial cells and podocytes

Our findings reveal a novel pathogenic mechanism of DN in which IL-6 released from glucose-stressed PTECs activates Rab5 signaling in podocytes, followed by nephrin endocytosis and structural injury of podocytes. Importantly, NMN treatment effectively disrupted this pathological pathway of intercellular communication, and provided significant protection against DN progression. These results suggest that NMN supplementation and targeting the IL-6/Rab5 signaling axis has promise as a therapeutic strategy for managing DN.