ReviewFrontiers in immunology2026
From local lesion to multisystem disease: integrated crosstalk among the gut microbiota, immune system, and host metabolism in endometriosis.
Review in Frontiers in immunology, 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
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
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
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometriosis (EMs) is a common estrogen-dependent inflammatory disease characterized by pelvic pain and infertility. Despite its substantial clinical burden, its etiology and pathogenesis remain incompletely resolved, and current management continues to be constrained by delayed diagnosis, limited therapeutic efficacy, and frequent disease recurrence. Growing evidence indicates that EMs is not merely a localized gynecological disorder but a disease state with multisystem pathophysiological features, a condition defined by crosstalk among the gut microbiota, the immune system, and host metabolism. This review synthesizes current evidence to establish a systems biology framework in which gut dysbiosis, immune dysfunction, and metabolic reprogramming are integrated as interconnected drivers of disease initiation, progression, and persistence. We first examine alterations in gut microbial composition and function, including estrogen metabolism dysregulation, expansion of opportunistic pathogens, and impaired intestinal barrier integrity, and discuss how these changes influence estrogen homeostasis, inflammatory signaling, and host-microbe interactions. We then explore how aberrations in innate and adaptive immunity promote immune evasion, chronic inflammation, angiogenesis, and ectopic lesion survival. Furthermore, we highlight the multifaceted remodeling of carbohydrate, lipid, and amino acid metabolism, and its link to cell proliferation and the immunosuppressive microenvironment. Particular emphasis is placed on the bidirectional interplay among microbial metabolites, immunometabolic signaling, oxidative stress, and tricarboxylic acid cycle (TCA) intermediates, all of which coalesce into a self-reinforcing pathological network. By integrating these domains, This review advances a unifying "microbiome-immune-metabolic" framework to elucidate the multisystem pathophysiological features of EMs, aiming to inspire the discovery of non-invasive biomarkers and the development of precision therapeutic strategies that target microbial, immune, and metabolic pathways.
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.