©The Author(s) 2025.
World J Diabetes. Oct 15, 2025; 16(10): 109782
Published online Oct 15, 2025. doi: 10.4239/wjd.v16.i10.109782
Published online Oct 15, 2025. doi: 10.4239/wjd.v16.i10.109782
Figure 8 Possible mechanism of crosstalk between proximal tubular epithelial cells and podocytes and effect of nicotinamide mo nonucleotide during diabetic nephropathy.
High-dose glucose induces the epithelial-mesenchymal transition and secretion of IL-6 by proximal tubular epithelial cells (PTECs). Podocytes sense this IL-6, and this leads to the binding of internalized nephrin with active Rab5, followed by disruptions of the cytoskeleton, podocyte adhesion, and podocyte spreading. nicotinamide mononucleotide blocks signaling from the PTECs, decreases the binding of nephrin with active Rab5, and ameliorates cellular damage. EMT: Epithelial-mesenchymal transition; NMN: Nicotinamide mononucleotide.
- Citation: Zha DQ, Gao P, Wu XY. Nicotinamide mononucleotide protects against diabetic nephropathy via IL-6/Rab5-mediated crosstalk between proximal tubular epithelial cells and podocytes. World J Diabetes 2025; 16(10): 109782
- URL: https://www.wjgnet.com/1948-9358/full/v16/i10/109782.htm
- DOI: https://dx.doi.org/10.4239/wjd.v16.i10.109782