©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 1 High-dose glucose-induced nephrin endocytosis promotes podocyte injury and endocytosis inhibitors block this effect.
A and B: Western blot analysis of cytoplasmic nephrin, membrane nephrin, and total nephrin in podocytes after different treatments and densitometric quantification of these results (n = 3); C: Representative confocal microscopy images of podocytes after different treatments (magnification: × 1000; scale bar: 50 μm; blue: Nuclei; red: Cytoskeleton); D: Adhesion of podocytes after different treatments (n = 3); E and F: Representative electron microscopy images of podocyte spreading after different treatments (magnification: × 400; scale bar: 20 μm) and quantification of these results (n = 3). aP < 0.05; bP < 0.001. HG: High-dose glucose.
- 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