©The Author(s) 2025.
World J Diabetes. Nov 15, 2025; 16(11): 111223
Published online Nov 15, 2025. doi: 10.4239/wjd.v16.i11.111223
Published online Nov 15, 2025. doi: 10.4239/wjd.v16.i11.111223
Figure 2 Ribonucleotide reductase regulatory subunit M2 overexpression increased the proliferation of high glucose-treated renal tubular cells.
HK-2 cells were treated with 5.5, 10, 20, 30, and 50 mmol/L D-glucose for 48 hours. A: Ribonucleotide reductase regulatory subunit M2 (RRM2) mRNA expression was determined using reverse transcription quantitative PCR (RT-qPCR); B: Representative gel blots of RRM2 obtained by Western blotting; C: RRM2 protein blots were quantified by normalizing to GAPDH; D and E: HK-2 cells were transfected with pCDH-CMV-RRM2 or an empty vector, and RT-qPCR and Western blotting were performed 48 hours after transfection; F: HK-2 cells were transfected with pCDH-CMV-RRM2 or an empty vector and treated with high glucose (HG; 30 mmol/L) for 48 hours. The effect of RRM2 overexpression on cell viability was assessed using MTT assay. Data are presented as mean ± SD in triplicate and analyzed using one-way ANOVA. aP < 0.001 vs HG (5.5 mM) group or control group; bP < 0.001 vs HG + vector. RRM2: Ribonucleotide reductase regulatory subunit M2; HG: High glucose; OE-RRM2: Overexpressing ribonucleotide reductase regulatory subunit M2.
- Citation: Gao CC, Ding FF, Jiang X. RRM2 attenuates the renal tubular ferroptosis in diabetic kidney disease through PI3K/Akt/Nrf2 pathway. World J Diabetes 2025; 16(11): 111223
- URL: https://www.wjgnet.com/1948-9358/full/v16/i11/111223.htm
- DOI: https://dx.doi.org/10.4239/wjd.v16.i11.111223