Endometrial cellular senescence contributes to preterm birth
نویسنده
چکیده
Preterm birth is a major global health issue, and its causes and underlying mechanism remain obscure. We recently established a mouse model of spontaneous preterm birth. In this model, endometrial cellular senescence early in pregnancy via mTORC1-p21 signaling is a major contributor of preterm birth and fetal death, and these adverse phenotypes are restored by the inhibition of mTORC1 or p21. This role of endometrial cellular senescence in determining the timing of birth in mouse models may help us better understand the mechanism of the timing of birth in humans and develop new and improved strategies against preterm birth. Rec.11/4/2013, Acc.12/16/2013, pp64-68
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