ReviewExpert opinion on therapeutic targets2016
p38 Mitogen activated protein kinase (MAPK): a new therapeutic target for reducing the risk of adverse pregnancy outcomes.
Review in Expert opinion on therapeutic targets, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 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
- Transcriptomic Reprogramming of the Human Placenta Following Maternal Opioid Exposure: Identification of Altered Metabolic and Translational Pathways.Current issues in molecular biology · 2026Article
- The Role of Papaverine in the Molecular and Biomechanical Mechanisms of Cervical Ripening: A Narrative Review.International journal of molecular sciences · 2026Review
- Heterogeneity in inflammatory responses to endotoxin at the fetomaternal interface.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Review
- Maternal urinary metabolomic signatures preceding spontaneous preterm birth: A pilot study.Scientific reports · 2025Article
- 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
- Exosomal delivery of IL-10: Biodistribution, pharmacokinetics, and preterm birth prevention strategies.Extracellular vesicle · 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
- The role of amniotic epithelial cells in preterm birth: mechanisms and clinical implications.Frontiers in cell and developmental biology · 2025Review
- Review
- Combined Application of Exosomes and FPR2 Agonist LXA4 in Controlling Fetal Membrane Inflammation and Promoting Fetal Membrane Tissue Repair.Reproductive sciences (Thousand Oaks, Calif.) · 2023Article
- Chromogranin A: An Endocrine Factor of Pregnancy.International journal of molecular sciences · 2023Review
- Stress signaler p38 mitogen-activated kinase activation: a cause for concern?Clinical science (London, England : 1979) · 2022Article
- Fetal membrane at the feto-maternal interface: An underappreciated and understudied intrauterine tissue.Placenta and reproductive medicine · 2022Article
- Computational Screening of the Natural Product Osthole and Its Derivates for Anti-Inflammatory Activity.Life (Basel, Switzerland) · 2022Article
- Actions of Bisphenol A on Different Feto-Maternal Compartments Contributing to Preterm Birth.International journal of molecular sciences · 2022Review
- Transcriptome Comparison of Chorion-Attached and Non-chorion-attached Endometrium in Mid-gestation of Rabbit.Frontiers in veterinary science · 2022Article
- TBX2, a Novel Regulator of Labour.Medicina (Kaunas, Lithuania) · 2021Article
- Aerobic Vaginitis Induced byFrontiers in microbiology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
introductionSpontaneous preterm birth (PTB) and preterm premature rupture of the membranes (pPROM) remain as a major clinical and therapeutic problem for intervention and management. Current strategies, based on our knowledge of pathways of preterm labor, have only been effective, in part, due to major gaps in our existing knowledge of risks and risk specific pathways. Areas covered: Recent literature has identified physiologic aging of fetal tissues as a potential mechanistic feature of normal parturition. This process is affected by telomere dependent and p38 mitogen activated protein kinase (MAPK) induced senescence activation. Pregnancy associated risk factors can cause pathologic activation of this pathway that can cause oxidative stress induced p38 MAPK activation leading to senescence and premature aging of fetal tissues. Premature aging is associated with sterile inflammation capable of triggering preterm labor or preterm premature rupture of membranes. Preterm activation of p38MAPK can be considered as a key contributor to adverse pregnancies. Expert opinion: This review considers p38MAPK activation as a potential target for therapeutic interventions to prevent adverse pregnancy outcomes mediated by stress factors. In this review, we propose multiple strategies to prevent p38MAPK activation.
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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.