ArticleAging2016
Placental membrane aging and HMGB1 signaling associated with human parturition.
Article in Aging, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
94 citing papers in PubMed, 1 synthesis or guideline pooled it, 142 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
- High-mobility group box 1 at the time of parturition in women with gestational diabetes mellitus.American journal of reproductive immunology (New York, N.Y. : 1989) · 2019Trial
- Aberrant expression of Gremlin1 induces trophoblast senescence in the placenta of advanced maternal age pregnancy.Journal of translational medicine · 2026Article
- The research on the relationship between mesenchymal stromal cell exosomes and recurrent spontaneous abortion.Archives of gynecology and obstetrics · 2026Review
- Translating cellular senescence research into clinical practice for metabolic disease.Nature reviews. Endocrinology · 2026Review
- A call to standardize the nomenclature of human fetal membrane at the feto-maternal interface.Placenta · 2025Review
- How aging causes osteoarthritis: An evolutionary physiology perspective.Osteoarthritis and cartilage · 2025Review
- Review
- 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
- Chorionic trophoblast cells demonstrate functionally different phenotypes from placental trophoblasts†.Biology of reproduction · 2025Article
- SenNet recommendations for detecting senescent cells in different tissues.Nature reviews. Molecular cell biology · 2024Review
- Role of the GalNAc-galectin pathway in the healing of premature rupture of membranes.Molecular medicine (Cambridge, Mass.) · 2024Article
- High-Throughput 3D-Printed Model of the Feto-Maternal Interface for the Discovery and Development of Preterm Birth Therapies.ACS applied materials & interfaces · 2024Article
- 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
- Relationship among α‑synuclein, aging and inflammation in Parkinson's disease (Review).Experimental and therapeutic medicine · 2024Review
- Autophagy Determines Distinct Cell Fates in Human Amnion and Chorion Cells.Autophagy reports · 2024Article
- Blockade of IL-6R prevents preterm birth and adverse neonatal outcomes.EBioMedicine · 2023Article
- 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
- Mitigating Oxidative Stress in Perinatal Cells: A Critical Step toward an Optimal Therapeutic Use in Regenerative Medicine.Biomolecules · 2023Review
34 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aging is associated with the onset of several diseases in various organ systems; however, different tissues may age differently, rendering some of them dysfunctional sooner than others. Placental membranes (fetal amniochorionic membranes) protect the fetus throughout pregnancy, but their longevity is limited to the duration of pregnancy. The age-associated dysfunction of these membranes is postulated to trigger parturition. Here, we investigated whether cellular senescence-the loss of cell division potential as a consequence of stress-is involved in placental membrane function at term. We show telomere reduction, p38 MAPK activation, increase in p21 expression, loss of lamin B1 loss, increase in SA-β-galactosidase , and senescence-associated secretory phenotype (SASP) gene expression in placental membranes after labor and delivery (term labor [TL]) compared to membranes prior to labor at term (term, not-in-labor [TNIL]). Exposing TNIL placental membranes to cigarette smoke extract, an oxidative stress inducer, also induced markers of cellular senescence similar to those in TL placental membranes. Bioinformatics analysis of differentially expressed SASP genes revealed HMGB1 signaling among the top pathways involved in labor. Further, we show that recombinant HMGB1 upregulates the expression of genes associated with parturition in myometrial cells. These data suggest that the natural physiologic aging of placental tissues is associated with cellular senescence and human parturition.
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What OpenQuestion holds
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.