ReviewObstetrics & gynecology science2019
Initiation of human parturition: signaling from senescent fetal tissues via extracellular vesicle mediated paracrine mechanism.
Review in Obstetrics & gynecology science, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
46 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.
- Cervical pessary to prevent preterm birth in asymptomatic high-risk women: a systematic review and meta-analysis.American journal of obstetrics and gynecology · 2020Pooled it
- Soluble P2X7 receptor (sP2X7R) as a marker of inflammation in pregnancy.Purinergic signalling · 2026Article
- Characteristics, Epigenetics, and Management of Non-Infectious Preterm Birth-Sterile Intrauterine Inflammation and Idiopathic Preterm Birth.Life (Basel, Switzerland) · 2026Review
- Heat-Induced Pathophysiological and Metabolic Changes at the Feto-Maternal Interface Predisposing to Preterm Birth.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Decidual Cells Induce Release of Free and Exosome-Bound Interferon Epsilon From Vaginal Epithelial Cells.American journal of reproductive immunology (New York, N.Y. : 1989) · 2025Article
- Review
- Exposure to Extreme Heat Increases Preterm Birth Risk: Hypothetical Pathophysiological Mechanisms.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- The Profile of Selected Protein Markers of Senescence in the Placentas of Cows During Early-Mid-Pregnancy and Parturition with and Without the Retention of Fetal Membranes: A Preliminary Study.International journal of molecular sciences · 2025Article
- Do progesterone receptor membrane components (PGRMC)s play a role in the chorions refractoriness to epithelial-to-mesenchymal transition (EMT)?Journal of reproductive immunology · 2025Article
- The role of amniotic epithelial cells in preterm birth: mechanisms and clinical implications.Frontiers in cell and developmental biology · 2025Review
- Distinct miRNA profiles in human amniotic tissue and its vesicular and non-vesicular secretome.Frontiers in cell and developmental biology · 2025Article
- miR-548az-5p induces amniotic epithelial cell senescence by regulating KATNAL1 expression in labor.Scientific reports · 2024Article
- Review
- Group B streptococcus induces cellular senescence in human amnion epithelial cells through a partial interleukin-1-mediated mechanism.Biology of reproduction · 2024Article
- Cargo exchange between human and bacterial extracellular vesicles in gestational tissues: a new paradigm in communication and immune development.Extracellular vesicles and circulating nucleic acids · 2024Review
- Is human labor at term an inflammatory condition?†.Biology of reproduction · 2023Review
- Deleterious and Protective Psychosocial and Stress-Related Factors Predict Risk of Spontaneous Preterm Birth.American journal of perinatology · 2023Article
- Stress signaler p38 mitogen-activated kinase activation: a cause for concern?Clinical science (London, England : 1979) · 2022Article
- Testing of drugs using human feto-maternal interface organ-on-chips provide insights into pharmacokinetics and efficacy.Lab on a chip · 2022Article
- Fetal membrane at the feto-maternal interface: An underappreciated and understudied intrauterine tissue.Placenta and reproductive medicine · 2022Article
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
Abstract
A better understanding of the underlying mechanisms by which signals from the fetus initiate human parturition is required. Our recent findings support the core hypothesis that oxidative stress (OS) and cellular senescence of the fetal membranes (amnion and chorion) trigger human parturition. Fetal membrane cell senescence at term is a natural physiological response to OS that occurs as a result of increased metabolic demands by the maturing fetus. Fetal membrane senescence is affected by the activation of the p38 mitogen activated kinase-mediated pathway. Similarly, various risk factors of preterm labor and premature rupture of the membranes also cause OS-induced senescence. Data suggest that fetal cell senescence causes inflammatory senescence-associated secretory phenotype (SASP) release. Besides SASP, high mobility group box 1 and cell-free fetal telomere fragments translocate from the nucleus to the cytosol in senescent cells, where they represent damage-associated molecular pattern markers (DAMPs). In fetal membranes, both SASPs and DAMPs augment fetal cell senescence and an associated 'sterile' inflammatory reaction. In senescent cells, DAMPs are encapsulated in extracellular vesicles, specifically exosomes, which are 30-150 nm particles, and propagated to distant sites. Exosomes traffic from the fetus to the maternal side and cause labor-associated inflammatory changes in maternal uterine tissues. Thus, fetal membrane senescence and the inflammation generated from this process functions as a paracrine signaling system during parturition. A better understanding of the premature activation of these signals can provide insights into the mechanisms by which fetal signals initiate preterm parturition.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.