Fig. 6. Fbf1 ablation protects mice from IR-induced senescence and associated frailty.

a Representative images of mice 3 months after IR. b The change in body weight of mice with 3 months after IR. n = 10 mice. c at 2 weeks after IR, liver was analyzed by immunohistochemistry using Il1α antibody or p16 antibody and quantified; Scale bar: 200 µm. n >80 cells were counted in n = 5 different fields in n = 3 mice’s Il1α staining and n = 8 different fields in n = 4 mice’s p16 staining d, e Lysates obtained from lung (d) and fat (e) tissue of WT mice, or Fbf1^tm1a/tm1a mice 2 weeks after IR were analyzed for the indicated proteins by western blot. f, g SASP-related genes were assessed by RT-qPCR in extracts of lung (f) and fat (g) tissue of WT mice or Fbf1^tm1a/tm1a mice 2 weeks after IR. n = 8 mice. Results from 3 independent experiments were statistically analyzed and plotted as means ± SEM. h–j Maximal speed (h), grip strength (i) and treadmill endurance (j) of 12-month-old WT mice or Fbf1^tm1a/tm1a C57BL/6 mice, 6 months after exposure to mock or sublethal dose of total-body IR (n = 10 for both groups, 5 males and 5 females). Values are expressed as means ± SEMs. Two-tailed Student’s unpaired t-test was used for analysis in a, c, f and g. One-way ANOVA followed by Bonferroni multiple-comparison analysis was employed for h–j. Source data are provided as a Source Data file.