The accumulation of senescent cells in the body is a hallmark of aging. These cells produce disruptive signaling that contributes to degenerative aging, impacting tissue structure and function. Signaling from other senescent cells and various forms of stress can induce bystander senescence, further adding to the burden of senescent cells. Current research suggests that soluble elements in the body can induce bystander senescence, and the identification of these components is essential for the development of senolytic therapies. In vivo studies are crucial for confirming the physiological relevance of senescence and understanding the mechanisms of induction. Armed with this knowledge, new strategies can be developed to mitigate the adverse effects of senescent cells on an organism’s health.
The characterization of age-altered contents in vesicles and aggregates, as well as the mechanisms of their uptake, is an essential but challenging endeavor. Understanding this field will be invaluable for the development of senolytic therapies that can prevent an organism-wide loss of health due to senescence propagation.
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