Figure 6.

Illustration summarizing the key points of our findings. The accumulation of senescent cells is one of the causative processes of aging, while the aging of tissues and organs also promotes the accumulation of SCs. CAG selectively induces SCs apoptosis via inhibition of Bcl-2 and the PI3K/AKT/mTOR pathway. CAG also suppresses the development of the SASP in SCs, thereby inhibiting cell senescence which is mediated by the SASP. CAG alleviated the SCs burden and improved age-related physical dysfunction in TBI-aged mice. Therefore, the senolytic agent CAG has the potential to be used in the treatment of age-related diseases. (CAG: cycloastragenol; NC: nonsenescent cells; SCs: senescent cells; SASP: senescence-associated secretory phenotype, e.g.,: intragastrical administration; TBI: total-body irradiation; IAT: inguinal adipose tissue).