Cellular senescence is a fundamental mechanism of aging characterised by a stable arrest of the cell cycle in response to stressors such as DNA damage, telomere shortening, and oncogenic signalling. While this process initially serves beneficial roles in tumour suppression, wound healing, and embryonic development, the accumulation of senescent cells over time drives tissue dysfunction and chronic diseases. A primary driver of this pathology is the senescence-associated secretory phenotype (SASP), a complex mix of pro-inflammatory cytokines, chemokines, and proteases secreted by senescent cells that triggers chronic sterile inflammation—often termed 'inflammaging'—and damages neighbouring tissues. The 'Geroscience Hypothesis' posits that targeting these fundamental aging mechanisms can delay the onset of multiple age-related comorbidities simulta ...