ReviewMolecular biology reports2026
Recent insights in pathogenesis of endometriosis with focus on gut microbiota.
Review in Molecular biology reports, 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
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
EMs is a chronic, estrogen-dependent systemic inflammatory disorder defined by the ectopic implantation of endometrial glands and stroma and is frequently associated with dysmenorrhea, chronic pelvic pain, infertility, and substantial impairment in quality of life. Despite its high prevalence and socioeconomic burden, the etiopathogenesis of EMs remains incompletely elucidated and appears to involve intricate interactions among endocrine dysregulation, immune dysfunction, epigenetic reprogramming, ferroptosis, miRNA-mediated gene regulation, environmental exposures, and lifestyle-related factors. Accumulating evidence has increasingly implicated GM dysbiosis in EMs development and progression. Alterations in microbial diversity and composition have been associated with changes in host immune homeostasis, estrogen metabolism, intestinal barrier integrity, inflammatory signaling cascades, microbial-derived metabolites, and gut-brain axis communication, which may foster a pro-inflammatory pelvic microenvironment that in turn may facilitate lesion implantation, angiogenesis, neuroinflammation, and pain sensitization. Elevated lipopolysaccharide levels, reduced short-chain fatty acid production, Th17/Treg imbalance, macrophage polarization, and epigenetic modulation have also been associated with GM perturbations in EMs. This review synthesizes current advances in understanding the multifactorial mechanisms underlying EMs pathogenesis, with a particular emphasis on microbiota-host interactions. We also discuss emerging microbiota-targeted therapeutic strategies, including probiotics, dietary modulation, and fecal microbiota transplantation, highlighting their translational potential as adjunctive approaches for disease management and personalized medicine in EMs.
Indexed as
Identifiers
42550338What Socratic 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 Socratic graph.