ReviewSeminars in immunopathology2020
Novel pathways of inflammation in human fetal membranes associated with preterm birth and preterm pre-labor rupture of the membranes.
Review in Seminars in immunopathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 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
73 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.
- Effects of vitamin D in pregnancy on maternal and offspring health-related outcomes: An umbrella review of systematic review and meta-analyses.Nutrition & diabetes · 2024Pooled it
- The Significance of YKL-40, a Marker Involved in Extracellular Matrix Remodeling, in Preterm Prelabor Rupture of Membranes: A Prospective Observational Study.Diagnostics (Basel, Switzerland) · 2026Article
- Prediction of premature rupture of fetal membranes using deep learning in East China.Scientific reports · 2026Article
- Exposure to traffic-related air pollution and the risk of premature rupture of membranes: a cohort analysis of the Korean CHildren's ENvironmental health Study (Ko-CHENS).Environmental science and pollution research international · 2026Article
- Heterogeneity in inflammatory responses to endotoxin at the fetomaternal interface.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Relationship between the dietary inflammatory index and immune function during pregnancy - A secondary analysis of the MicrobeMom2 Study.European journal of clinical nutrition · 2026Article
- Endocrine Disruptors at the Fetomaternal Interface: Insight From PBDE Studies and the Utility of Novel Approach Methods.Endocrinology · 2026Review
- Comparative Effectiveness of Azithromycin versus Erythromycin for Latency Prolongation in Preterm Prelabor Rupture of Membranes < 34 Weeks of Gestation.International journal of women's health · 2026Article
- The Role of the Vaginal Microbiome in Preterm Premature Rupture of Membranes: A Comprehensive Review of Mechanisms and Clinical Implications.Health science reports · 2025Article
- Biomaterials for fetal membrane repair in preterm premature rupture of membranes: advances in tissue engineering strategies.Journal of biological engineering · 2025Review
- Unveiling the vital role of OGG1 in inflammation, vascular endothelial damage, and cell death in obstetric and gynecological diseases.Human cell · 2025Review
- Hierarchical metal exposure in umbilical cord blood in relation to oxidative stress and AMPK/NF-κB signaling in preterm membrane rupture.Scientific reports · 2025Article
- Review
- Exposure to Extreme Heat Increases Preterm Birth Risk: Hypothetical Pathophysiological Mechanisms.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Placental Inflammation in Preterm Premature Rupture of Membranes and Risk of Neurodevelopmental Disorders.Cells · 2025Review
- Impact of short-term air pollution exposure on premature rupture of membranes in the North China Plain, 2015-2021: a multicity case-crossover study.Journal of global health · 2025Article
- Intermediate Signaling Mechanisms Regulating Human Fetal Membrane Responses to Gram-Positive Bacterial Peptidoglycan.American journal of reproductive immunology (New York, N.Y. : 1989) · 2025Article
- The Impacts of TNF-α-Induced Inflammation on Amnion Epithelial Cells: Exploring Stem Cell Gene Expression, Senescence, Inflammatory Responses, and Cellular Transition.American journal of reproductive immunology (New York, N.Y. : 1989) · 2025Article
- Mapping genetic susceptibility to spontaneous preterm birth: analysis of Utah pedigrees to find inherited genetic factors.American journal of obstetrics and gynecology · 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
13 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
4 authors at 3 institutions in 2 countries.
Funding
Abstract
Spontaneous preterm birth (PTB) and preterm pre-labor rupture of the membranes (pPROM) are major pregnancy complications. Although PTB and pPROM have common etiologies, they arise from distinct pathophysiologic pathways. Inflammation is a common underlying mechanism in both conditions. Balanced inflammation is required for fetoplacental growth; however, overwhelming inflammation (physiologic at term and pathologic at preterm) can lead to term and preterm parturition. A lack of effective strategies to control inflammation and reduce the risk of PTB and pPROM suggests that there are several modes of the generation of inflammation which may be dependent on the type of uterine tissue. The avascular fetal membrane (amniochorion), which provides structure, support, and protection to the intrauterine cavity, is one of the key contributors of inflammation. Localized membrane inflammation helps tissue remodeling during pregnancy. Two unique mechanisms that generate balanced inflammation are the progressive development of senescence (aging) and cyclic cellular transitions: epithelial to mesenchymal (EMT) and mesenchymal to epithelial (MET). The intrauterine build-up of oxidative stress at term or in response to risk factors (preterm) can accelerate senescence and promote a terminal state of EMT, resulting in the accumulation of inflammation. Inflammation degrades the matrix and destabilizes membrane function. Inflammatory mediators from damaged membranes are propagated via extracellular vesicles (EV) to maternal uterine tissues and transition quiescent maternal uterine tissues into an active state of labor. Membrane inflammation and its propagation are fetal signals that may promote parturition. This review summarizes the mechanisms of fetal membrane cellular senescence, transitions, and the generation of inflammation that contributes to term and preterm parturitions.
Indexed as
Identifiers
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.