ArticlePlacenta2016
Differential senescence in feto-maternal tissues during mouse pregnancy.
Article in Placenta, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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.
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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
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 85 citations in OpenAlex.
- Systematic review of p38 mitogen-activated kinase and its functional role in reproductive tissues.American journal of reproductive immunology (New York, N.Y. : 1989) · 2018Pooled it
- Selective Targeting of Senescent FHs74Int Cells by Human Breast Milk Free Fatty Acids.Biology · 2025Article
- Regulatory Interplay of p53, AMPK, and mTOR in Decidualization: Implications for Reproductive Competence and Cancer Biology.Reproductive sciences (Thousand Oaks, Calif.) · 2025Review
- 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
- Lead exposure at the feto-maternal interface: a cause for concern for fetal membrane trophoblasts.Toxicological sciences : an official journal of the Society of Toxicology · 2025Article
- SenNet recommendations for detecting senescent cells in different tissues.Nature reviews. Molecular cell biology · 2024Review
- Frontiers in the Etiology and Treatment of Preterm Premature Rupture of Membrane: From Molecular Mechanisms to Innovative Therapeutic Strategies.Reproductive sciences (Thousand Oaks, Calif.) · 2024Review
- Linking DNA damage and senescence to gestation period and lifespan in placental mammals.Frontiers in cell and developmental biology · 2024Article
- Hypoxia-inducible factor 1 signaling drives placental aging and can provoke preterm labor.eLife · 2023Article
- Evidence of Placental Aging in Late SGA, Fetal Growth Restriction and Stillbirth-A Systematic Review.Biomedicines · 2023Review
- Is human labor at term an inflammatory condition?†.Biology of reproduction · 2023Review
- Stress signaler p38 mitogen-activated kinase activation: a cause for concern?Clinical science (London, England : 1979) · 2022Article
- Fetal inflammatory response at the fetomaternal interface: A requirement for labor at term and preterm.Immunological reviews · 2022Review
- The immunobiology of preterm labor and birth: intra-amniotic inflammation or breakdown of maternal-fetal homeostasis.Reproduction (Cambridge, England) · 2022Review
- Leukocyte telomere dynamics across gestation in uncomplicated pregnancies and associations with stress.BMC pregnancy and childbirth · 2022Article
- Fetal Lung-Derived Exosomes in Term Labor Amniotic Fluid Induce Amniotic Membrane Senescence.Frontiers in cell and developmental biology · 2022Article
- Advanced maternal age induces fetal growth restriction through decreased placental inflammatory cytokine expression and immune cell accumulation in mice.The Journal of reproduction and development · 2021Article
- Extracellular vesicle mediated feto-maternal HMGB1 signaling induces preterm birth.Lab on a chip · 2021Article
- Molecular Pathways of Cellular Senescence and Placental Aging in Late Fetal Growth Restriction and Stillbirth.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundHuman studies show that fetal membranes have a limited lifespan and undergo telomere-dependent cellular senescence that is augmented by oxidative stress and mediated by p38 mitogen activated protein kinase (MAPK). Further, these studies suggest that fetal membranes are anatomically and physiologically positioned to transmit senescence signals that may initiate parturition at term.
methodsLongitudinal evaluation of feto-maternal tissues from mouse pregnancies was undertaken to determine the molecular progression of senescence during normal pregnancy. On days 10-18 of gestation, C57BL/6 mice were euthanized. Fetal membranes, placenta, and decidua/uterus were collected. Tissues were examined for Telomere length (TL) and the presence of Phosphorylated (P) p38MAPK and p53, p21 and senescence associated β-Galactosidase (SA- β-Gal).
findingsLinear regression modeling of observed telomere length as a function of gestational age revealed that beta (β), the slope of the linear regression was negative and significantly different from zero for each tissue (fetal membranes, β = -0.1901 ± 0.03125, p < 0.0001; placenta β = -0.09000 ± 0.03474, p = 0.0135; decidua/uterus β = -0.1317 ± 0.03264, p = 0.0003). Progressive activation p38MAPK was observed in all tissues from days 10 to day18, with the highest activation observed in fetal membranes. Activation of p53 was progressive in fetal membranes. In contrast, active p53 was constitutive in placenta and decidua/uterus throughout gestation. Detection of p21 indicated that pro-senescent change was higher in all compartments on day 18 as compared to other days. The number of SA-β-Gal positive cells increased in fetal membranes as gestation progressed. However, in placenta and uterus and decidua/uterus SA-β-Gal was seen only in days 15 and 18.
conclusionsTelomere dependent p38 and p53 mediated senescence progressed in mouse fetal membranes as gestation advanced. Although senescence is evident, telomere dependent events were not dominant in placenta or decidua/uterus. Fetal membrane senescence may significantly contribute to mechanisms of parturition at term.
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