Skip to main content
. Author manuscript; available in PMC: 2018 Mar 23.
Published in final edited form as: Cell. 2017 Mar 23;169(1):132–147.e16. doi: 10.1016/j.cell.2017.02.031

Fig. 7. By targeting senescence, FOXO4-DRI counters frailty and loss of renal function in naturally aged p16∷3MR mice.

Fig. 7

A) Quantification of p16ink4a-driven RLUC radiance in 104w old p13∷3MR mice compared to 26w counterparts. Note there is a larger degree of spread in the signal, suggesting biological variation. B) Quantification of the % platelets at time of sacrifice/baseline of naturally aged p16∷3MR mice treated with PBS or FOXO4-DRI for 30d. Procedure as in Fig. 5C. C) Representative images and quantification of p16ink4a-driven RLUC radiance of mice the from B). D) Example of fur density in FOXO4-DRI vs. Mock-treated male p16∷3MR mice. See also Fig. S7B. E) Quantification of the responsiveness of the mice in B–D treated with FOXO4-DRI or PBS. Analysis as in Fig. 5F. F–I) Quantification of the effects of FOXO4-DRI on LMNB1 loss and IL6 intensity in the kidneys and plasma [Urea] and [Creatinine] of the naturally aged p16∷3MR mice from B). G) Quantification of % plasma [Urea] and [Creatinine] of naturally aged (110+wk) p16∷3MR mice at 30d after i.p. injection with 3× 5mg/kg (every other day) FOXO4-DRI or 5×25mg/kg/day with GCV to clear senescent cells semigenetically.