ArticleThe EMBO journal2024
TNFSF14
Article in The EMBO journal, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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
16 citing papers in PubMed.
- CD38-activated macrophages drive age-related placental senescence by depleting NADNature communications · 2026Article
- Article
- Metabolic Reprogramming at the Maternal-Fetal Interface: Insights from Decidual Stromal Cells and Trophoblasts in Healthy Pregnancy Versus Recurrent Pregnancy Loss.International journal of molecular sciences · 2026Review
- Trophoblast aging driven by IL33 deficiency elevates recurrent pregnancy loss risk through SNAP29 lactylation-mediated autophagy impairment.Autophagy · 2026Article
- Decidual aging in recurrent pregnancy Loss: from regulating networks to therapeutic interventions.npj aging · 2026Review
- Endometrial senescence: inevitability and conditional occurrence in female fertility.Reproduction & fertility · 2026Review
- Dysregulated landscape of RNA-binding proteins in unexplained recurrent spontaneous abortion revealed by bulk and single-cell transcriptome.Scientific reports · 2026Article
- Pathway-Level Convergence Between Dynamic Plasma miRNAs and Endometrial Biological Processes During the Human Peri-Implantation Window.International journal of molecular sciences · 2026Article
- Impaired BCAA Catabolism Contributes To Acute Lung Injury By Triggering Oxidative Stress and Inflammatory Response Via the MAPK Pathway.Inflammation · 2026Article
- ISENICS: a model for identifying senescent immune cells and samples and characterization of their roles in tumor microenvironment.Briefings in bioinformatics · 2025Article
- Cell cycle regulation by the ribotoxic stress response.Trends in cell biology · 2025Review
- Efficacy of Intravenous Immunoglobulin for Patients with Recurrent Miscarriage: A Meta-Analysis.Iranian journal of public health · 2025Review
- Branched-Chain Amino Acid Metabolic Reprogramming and Cancer: Molecular Mechanisms, Immune Regulation, and Precision Targeting.Oncology research · 2025Review
- Cellular Senescence in Endometrium: A Pivotal Regulator in Physiological Remodeling and Pathological Disorders.International journal of biological sciences · 2025Review
- Cellular senescence in the innervated niche modulates cancer-associated pain: an emerging therapeutic target?Frontiers in immunology · 2025Review
- Metabolomic analysis reveals potential role of immunometabolism dysregulation in recurrent pregnancy loss.Frontiers in endocrinology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
In preparation for a potential pregnancy, the endometrium of the uterus changes into a temporary structure called the decidua. Senescent decidual stromal cells (DSCs) are enriched in the decidua during decidualization, but the underlying mechanisms of this process remain unclear. Here, we performed single-cell RNA transcriptomics on ESCs and DSCs and found that cell senescence during decidualization is accompanied by increased levels of the branched-chain amino acid (BCAA) transporter SLC3A2. Depletion of leucine, one of the branched-chain amino acids, from cultured media decreased senescence, while high leucine diet resulted in increased senescence and high rates of embryo loss in mice. BCAAs induced senescence in DSCs via the p38 MAPK pathway. In contrast, TNFSF14+ decidual natural killer (dNK) cells were found to inhibit DSC senescence by interacting with its ligand TNFRSF14. As in mice fed high-leucine diets, both mice with NK cell depletion and Tnfrsf14-deficient mice with excessive uterine senescence experienced adverse pregnancy outcomes. Further, we found excessive uterine senescence, SLC3A2-mediated BCAA intake, and insufficient TNFRSF14 expression in the decidua of patients with recurrent spontaneous abortion. In summary, this study suggests that dNK cells maintain senescence homeostasis of DSCs via TNFSF14/TNFRSF14, providing a potential therapeutic strategy to prevent DSC senescence-associated spontaneous abortion.
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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.