ReviewiScience2026
Pyroptosis in endometritis: Molecular mechanisms, pathogenic roles, and therapeutic opportunities.
Review in iScience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometritis is a common inflammatory disorder of the female reproductive tract caused by microbial infection or immune dysregulation that impairs endometrial function and reproductive outcomes. Growing evidence indicates that programmed cell death (PCD), particularly pyroptosis, plays a pivotal role in the pathophysiology of endometritis. Pyroptosis links cell death to inflammatory signaling through inflammasome activation and gasdermin (GSDM)-mediated membrane perforation. The canonical NLRP3-caspase-1-GSDMD axis, the noncanonical caspase-4/5/11-GSDMD pathway, and caspase-3-GSDME-dependent pyroptosis-like death all have been implicated in amplifying endometrial inflammation. Experimental and clinical studies demonstrate the upregulation of NLRP3, caspase-1, and GSDMD in affected endometrial tissues, supporting their pathological relevance. Upstream mechanisms, including the high-mobility group box 1 (HMGB1)-TLR4 axis, PI3K-AKT signaling, and microRNA (miRNA)-mediated modulation, further regulate the pyroptotic response. These insights highlight therapeutic opportunities, including pharmacological inhibitors, miRNA-based interventions, and antioxidant strategies. Nevertheless, most evidence derives from preclinical studies, and translational validation in patients remains limited. This review presents an integrated molecular framework and candidate therapeutic targets to support diagnostic stratification and precision interventions that optimize reproductive outcomes.
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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.