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©The Author(s) 2025.
World J Diabetes. May 15, 2025; 16(5): 102994
Published online May 15, 2025. doi: 10.4239/wjd.v16.i5.102994
Published online May 15, 2025. doi: 10.4239/wjd.v16.i5.102994
Figure 2 FOXO1 knockdown activates autophagy to protect β-cells against high glucose-induced dysfunction.
sh-FOXO1 and/or the autophagy inhibitor 3-MA were used to treat high glucose-treated MIN6 cells. A and B: Reverse transcription quantitative polymerase chain reaction and western blotting were used to analyze FOXO1 mRNA and protein expression; C: EdU staining was used to analyze cell proliferation ability (red staining: the labeled proliferating cells, blue staining: the nuclei); D: Flow cytometry was used to assess the cell apoptosis rate; E: Insulin levels were measured via ELISA; F: The expression of the autophagy proteins LC3B and p62 was analyzed via western blotting. The data are expressed as mean ± SD. Each experiment was conducted in triplicate. aP < 0.05 vs control group, bP < 0.05 vs control group, cP < 0.05 vs HG + sh-NC group, dP < 0.05 vs HG + sh-FOXO1 group. HG: High glucose.
- Citation: Lei XT, Chen XF, Qiu S, Tang JY, Geng S, Yang GY, Wu QN. TERT/FOXO1 signaling promotes islet β-cell dysfunction in type 2 diabetes mellitus by regulating ATG9A-mediated autophagy. World J Diabetes 2025; 16(5): 102994
- URL: https://www.wjgnet.com/1948-9358/full/v16/i5/102994.htm
- DOI: https://dx.doi.org/10.4239/wjd.v16.i5.102994