Apheresis for senescence: Targeting the senescence-associated secretory phenotype to delay aging and age-related diseases.
Abstract
Aging is driven by cellular senescence and chronic inflammation, largely mediated by the senescence-associated secretory phenotype (SASP). SASP factors promote inflammaging, impair tissue homeostasis, and contribute to age-related diseases such as cardiovascular disease, neurodegeneration, and cancer. Current anti-aging strategies focus on senolytics or SASP inhibitors, yet these approaches have limitations. We discuss therapeutic plasma exchange (TPE) and selective apheresis, as interventions to mitigate SASP-driven aging. TPE removes inflammatory cytokines, metabolic waste, and senescence-associated proteins, while replenishing rejuvenating factors. Selective apheresis could enhance precision by targeting specific SASP components. By reducing systemic inflammation and restoring a youthful proteomic environment, these strategies may improve immune function, tissue regeneration, and overall healthspan. This review explores the mechanistic basis of SASP in aging and evaluates the potential of apheresis-based therapies as viable interventions to delay aging and age-related disease progression.
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Research summary
Therapeutic plasma exchange and selective apheresis can mitigate the effects of the senescence-associated secretory phenotype to delay aging and age-related diseases. The paper addresses the root causes of aging by targeting cellular senescence and chronic inflammation, which are central to the aging process and age-related diseases.
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