NR4A1 silencing alleviates high-glucose-stimulated HK-2 cells pyroptosis and fibrosis via hindering NLRP3 activation and PI3K/AKT pathway

doi:10.4239/wjd.v16.i3.97544

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World Journal of Diabetes

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Baishideng Publishing Group Inc, 7041 Koll Center Parkway, Suite 160, Pleasanton, CA 94566, USA

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World J Diabetes. Mar 15, 2025; 16(3): 97544
Published online Mar 15, 2025. doi: 10.4239/wjd.v16.i3.97544

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Figure 7 Diagram of possible mechanisms by which silencing of NR4A1 ameliorates diabetic kidney disease in vitro. HG: High glucose; AKT: Protein kinase B; PI3K: Phosphoinositide 3-kinase; si-NR4A1: SiRNA targeting nuclear receptor subfamily 4 group A member 1; TGF-β1: Transforming growth factor-β1; NLRP3: NOD-like receptor protein 3; GSDMD: Gasdermin D; IL-1β: Interleukin-1β.

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