Hormonal
Rapamycin inhibits the senescence-associated secretory phenotype (SASP) and reduces SA-β-gal staining in senescent cells through a mechanism independent of the Nrf2 pathway, likely involving Stat3 inhibition.
Rapamycin reduces the harmful inflammatory output (SASP) of aging cells without necessarily stopping them from dividing, and it does this via a pathway separate from the antioxidant response (Nrf2). This suggests that therapies targeting inflammation in aging might not need to address cell cycle arrest directly.
Our data thus suggest that cell senescence is a complex process that involves at least two arms, and rapamycin uses Nrf2 to regulate cell cycle arrest, but not the production of SASP.
Why this rating
Strong in vitro and in vivo evidence using multiple cell types and Nrf2 knockout models, though specific dosing in humans is not provided.
Source
Rapamycin inhibits the secretory phenotype of senescent cells by a Nrf2-independent mechanism
Rong Wang et al. · Aging Cell · 2017
DOI 10.1111/acel.12587
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