Throughout life, cells become senescent due to factors such as reaching the Hayflick limit or sustaining mutational damage. Senescent cells stop replicating and release pro-inflammatory signals, which can lead to tissue disruption. Introducing senescent cells into mice has been shown to accelerate aging-related conditions. A recent study found that transplanting senescent cells into the skin of young mice led to increased senescence in multiple tissues, frailty, musculoskeletal impairment, cognitive decline, and increased expression of senescence markers in the brain. This suggests that senescent cells in the skin can have systemic effects, impacting various organs and contributing to age-related decline. Future research should explore mechanisms and potential therapeutic interventions for senescent cell accumulation.