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Semin Perinatol. 2017 Nov;41(7):420-426. doi: 10.1053/j.semperi.2017.07.013. Epub 2017 Sep 8.

Pathophysiology of preterm labor with intact membranes.

Author information

1
Department of Obstetrics and Gynecology, University Hospitals Cleveland Medical Center, Cleveland OH.
2
Department of Obstetrics and Gynecology, University Hospitals Cleveland Medical Center, Cleveland OH; Department of Reproductive Biology, Case Western Reserve University, Cleveland, OH.
3
Department of Obstetrics and Gynecology, University Hospitals Cleveland Medical Center, Cleveland OH; Department of Reproductive Biology, Case Western Reserve University, Cleveland, OH. Electronic address: sam.mesiano@case.edu.

Abstract

Preterm labor with intact membranes is a major cause of spontaneous preterm birth (sPTB). To prevent sPTB a clear understanding is needed of the hormonal interactions that initiate labor. The steroid hormone progesterone acting via its nuclear progesterone receptors (PRs) in uterine cells is essential for the establishment and maintenance of pregnancy and disruption of PR signaling (i.e., functional progesterone/PR withdrawal) is key trigger for labor. The process of parturition is also associated with inflammation within the uterine tissues and it is now generally accepted that inflammatory stimuli from multiple extrinsic and intrinsic sources induce labor. Recent studies suggest inflammatory stimuli induce labor by affecting PR transcriptional activity in uterine cells to cause functional progesterone/PR withdrawal. Advances in understanding the functional interaction of inflammatory load on the pregnancy uterus and progesterone/PR signaling is opening novel areas of research and may lead to rational therapeutic strategies to effectively prevent sPTB.

KEYWORDS:

inflammation; parturition; pathophysiology; progesterone

PMID:
28889957
DOI:
10.1053/j.semperi.2017.07.013
[Indexed for MEDLINE]

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