Extracellular Vesicles Emerge as Key Drivers of Aging's Inflammatory Cascade

Senescent cells don't just sit passively; they actively spread damage through their senescence-associated secretory phenotype (SASP). This review in *Aging and Disease* highlights extracellular vesicles (EVs)—tiny membrane-bound packages of proteins, RNAs, and other molecules—as star players in this process. Unlike freely secreted SASP factors, EVs protect their cargo during transit and deliver it directly into recipient cells, amplifying inflammatory signals and spreading senescence to neighboring tissues. This mechanism helps explain "inflammaging," the chronic low-grade inflammation that drives many age-related diseases. The good news: EVs are also potential therapeutic targets. Blocking EV production or uptake might blunt SASP effects, while engineered EVs could deliver anti-aging treatments. The review synthesizes current knowledge on EV biology in aging and suggests both senolytics (which clear senescent cells) and EV-targeting strategies as promising interventions. As EV biology tools improve, this could open practical new routes to combat aging's inflammatory burden.