Abstract:
:Although preterm delivery is a major global health issue, its causes and underlying mechanism remain elusive. Using mutant mice, mimicking aspects of human preterm birth, we show here that uterine decidual senescence early in pregnancy via heightened mammalian target of rapamycin complex 1 (mTORC1) signaling is a significant contributor of preterm birth and fetal death, and that these adverse phenotypes are rescued by a low dose of rapamycin, an inhibitor of mTORC1 signaling. This role of mTORC1 signaling in determining the timing of birth in mice may help us better understand the mechanism of the timing of birth in humans and develop new and improved strategies to combat the global problem of preterm birth.
journal_name
Proc Natl Acad Sci U S Aauthors
Hirota Y,Cha J,Yoshie M,Daikoku T,Dey SKdoi
10.1073/pnas.1108180108subject
Has Abstractpub_date
2011-11-01 00:00:00pages
18073-8issue
44eissn
0027-8424issn
1091-6490pii
1108180108journal_volume
108pub_type
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