ArticleAging cell2026
Age-Associated Senescence of Decidual Macrophages: A Key Mediator of Adverse Pregnancy Outcomes in Advanced Maternal Age.
Article in Aging cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- The Role of Macrophages in Endometrial Cyclical Changes and Female Reproductive System Diseases: A Review.Current issues in molecular biology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Senescence of immune cells can drive senescence of solid organs, and reversing immune cell senescence ameliorates organismal senescence phenotypes. As the second largest subset of decidual immune cells, macrophages play a critical role in pregnancy. However, whether decidual macrophages (DM) exhibit senescence in advanced maternal age (AMA) pregnancies (≥ 35 years old) and their involvement in AMA-related adverse outcomes remain undefined. This study elucidates the phenotypic and functional characteristics of DM in AMA pregnancies through clinical samples, animal models, and in vitro experiments. It clarifies the mechanisms underlying DM aging and explores novel intervention strategies to reverse DM aging and improve pregnancy outcomes in AMA pregnancies. We found that the presence of DM senescence in AMA pregnancies, manifested by an increased proportion of the pro-inflammatory phenotype M1, increased expression of senescence markers (P53 and SA-β-Gal), and decreased phagocytic capacity-all associated with the development of adverse outcomes in AMA. The mechanistic basis of DM senescence involves two key pathways: on the one hand, low expression of forkhead box O3 causes DM senescence by downregulating mitophagy. On the other hand, elevated IL-6 in the uterine microenvironment exacerbates senescence. Adoptive transfer of young mouse bone marrow-derived macrophages significantly rescues embryo resorption rates and placental development in AMA pregnant mice. Overall, our study uncovers novel mechanisms and therapeutic strategies for AMA-related adverse pregnancy outcomes through a new perspective of uterine macrophage senescence, providing new intervention ideas to improve adverse pregnancy outcomes in AMA.
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.