Cellular aging shifts intercellular signaling from coordinated, functional communication toward chaotic, inflammatory crosstalk driven by the senescence-associated secretory phenotype (SASP). Senescent cells accumulate with age and release a cocktail of pro-inflammatory cytokines, proteases, and growth factors that corrupt neighboring tissue environments — a mechanism the authors frame as 'misdirected' rather than merely absent communication. The translational strategy under review involves senolytics (compounds that selectively eliminate senescent cells) and senomorphics (agents that suppress SASP without killing senescent cells), both showing promise in animal models awaiting human translation.
This synthesis arrives at a moment when the senolytic field is transitioning from rodent proof-of-concept to human clinical trials. Compounds like dasatinib combined with quercetin, and navitoclax, have demonstrated measurable reductions in senescent cell burden in early human studies, though long-term safety and efficacy data remain thin. The SASP framing matters because it repositions inflammaging — the chronic low-grade inflammation characteristic of aging — not as passive immune decline but as active, cell-generated signaling sabotage. That mechanistic distinction has real therapeutic implications: suppressing SASP without full senescent cell clearance may be sufficient to restore tissue homeostasis in some contexts. However, this is a narrative review-style article rather than original experimental research, and it does not present new primary data. Its value lies in contextualizing the senolytics-vs-senomorphics debate for a clinical geriatrics audience rather than advancing the mechanistic frontier.
