Fig. 8

Involvement of SETD7-p53-FBXO45-GPX4 axis in diabetic mice endothelial dysfunction. A The protein expression of p53, FBXO45, GPX4, and NOX4 in aortic tissues of WT and Setd7^−/− mice induced by STZ (50 mg/kg/d) for five consecutive days (n = 4). B Representative images of immunohistochemical FBXO45-stained thoracic aorta sections isolated from WT and Setd7^−/− mice. Scale bars, 50 μm. C Representative images of immunofluorescence GPX4-stained thoracic aorta sections isolated from WT and Setd7^−/− mice. Scale bars, 50 μm. D The protein expression of p53, FBXO45, GPX4, and NOX4 in aortic tissues of WT/WT and db/db mice received AAV-shSetd7 or AAV-Ctr (n = 4). E Representative images of immunohistochemical FBXO45-stained thoracic aorta sections isolated from WT/WT and db/db mice received AAV-shSetd7 or AAV-Ctr. Scale bars, 50 μm. F Representative images of immunofluorescence GPX4-stained thoracic aorta sections isolated from WT/WT and db/db mice received AAV-shSetd7 or AAV-Ctr. Scale bars, 50 μm. Statistical significances were calculated using (A and D) two-way ANOVA, Tukey’s multiple comparisons tests. Data are expressed as the mean ± SEM, statistical analysis revealed a significant difference with **p < 0.01, ***p < 0.001, #p < 0.05, ###p < 0.001