Articlenpj aging2026
FOSL2-driven SASP in endometrial stroma promotes the inflammation of endometriosis.
Article in npj aging, 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
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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
1 citing paper in PubMed.
- Mechanisms and Therapeutic Potential of Targeting Mitophagy in Neurodegenerative Diseases.Molecular neurobiology · 2026Review
Corrections and comments
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Authors and funding
9 authors.
Funding
Abstract
Endometriosis (EMs) is characterized by chronic pelvic inflammation, but the etiology of this inflammation remains poorly understood. The senescence-associated secretory phenotype (SASP), whereby senescent cells secrete pro-inflammatory cytokines, is a potential mechanism. This study investigates the pro-inflammatory SASP in EMs and its underlying influences. Through molecular assays and single-cell RNA-seq analysis, we found a subgroup of endometrial stromal cells (ESCs) marked by SASP in both eutopic endometrium and endometriotic lesions of EMs patients. The transcription factor FOSL2 was aberrantly overexpressed in this ESC subgroup; its overexpression induced cellular senescence and the secretion of SASP factors, while FOSL2 knockdown reversed these effects. Conditioned medium from ESCs with high FOSL2 expression promoted M2 macrophage polarization and recruitment. Mechanistically, FOSL2 overexpression in ESCs was regulated by the PGE2/cAMP/PKA signaling pathway, and FOSL2 modulated SASP through the activation of NF-κB signaling. In conclusion, the SASP in ESCs, regulated by FOSL2, contributes to chronic pelvic inflammation and immune system disruption in EMs patients. Targeting FOSL2 to reverse the SASP may offer a promising therapeutic strategy for EMs.
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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.