期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 108, 期 44, 页码 18073-18078出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1108180108
关键词
uterus; phospho-S6; p21; prostaglandins; parturition
资金
- Bill and Melinda Gates Foundation through the Grand Challenges Explorations Initiative
- National Institutes of Health [HD12304, DA06668]
- Precursory Research for Embryonic Science and Technology
- Uehara Memorial Foundation
- Takeda Science Foundation
- National Institute of Child Health and Development [T32 HD07463]
- National Institute on Aging [F30AG040858]
- Grants-in-Aid for Scientific Research [23890045] Funding Source: KAKEN
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.
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