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The proposed signaling pathway to preterm birth. Uterine deletion of p53 in mice results in increased PI3K-Akt signaling, which suppresses TSC activity by phosphorylating TSC2. Thus, TSC's inhibition on mTORC1 signaling is released, reflecting higher levels of pS6, as well as p21 levels. These changes give rise to heightened cellular senescence associated with increased PGF2α generation via the COX2-PGFS pathway, driving preterm birth.
