Copyright
©The Author(s) 2025.
World J Diabetes. Mar 15, 2025; 16(3): 97544
Published online Mar 15, 2025. doi: 10.4239/wjd.v16.i3.97544
Published online Mar 15, 2025. doi: 10.4239/wjd.v16.i3.97544
Figure 4 Markers of PI3K/AKT signaling pathway-mediated fibrosis were upregulated in rats with diabetic kidney disease.
A: Representative western blotting and integrated density study of AKT, p-AKT, PI3K, and p-PI3K in rat kidney tissues; B: Representative western blotting and integrated density study of TGF-β1 and collagen III in rat kidney tissue, n = 3. aP < 0.05 vs control. AKT: Protein kinase B; CON: Control; DKD: Diabetic kidney disease; PI3K: Phos phoinositide 3-kinase; TGF-β1: Transforming growth factor β1.
- Citation: Li JM, Song ZH, Li Y, Chen HW, Li H, Yuan L, Li J, Lv WY, Liu L, Wang N. NR4A1 silencing alleviates high-glucose-stimulated HK-2 cells pyroptosis and fibrosis via hindering NLRP3 activation and PI3K/AKT pathway. World J Diabetes 2025; 16(3): 97544
- URL: https://www.wjgnet.com/1948-9358/full/v16/i3/97544.htm
- DOI: https://dx.doi.org/10.4239/wjd.v16.i3.97544