ReviewiScience2026
Metabolic remodeling of endometriosis microenvironment: Energy stress and immune evasion.
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
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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endometriosis (EMs) is an estrogen-dependent chronic inflammatory gynecological disease characterized by ectopic growth of endometrial tissues, leading to dysmenorrhea, pelvic pain, and infertility. Although the retrograde menstruation theory clarifies the dissemination of endometrial fragments to ectopic sites, the mechanisms behind the survival of ectopic lesions and their immune evasion in hostile microenvironments remain unclear. Endometrial stromal cells (ESCs) are chronically exposed to a microenvironment of hypoxia, nutrient deprivation and oxidative stress, and this energy stress state drives the ESCs to develop adaptive metabolic reprogramming. Through remodeling glucose, lipid, and amino acid metabolic pathways, ESCs not only fulfill their own proliferative requirements but also utilize metabolites as signaling mediators to modulate immune cell functions. This review elaborates on the characteristics of energy stress-driven metabolic reprogramming in EMs, deciphers its mechanisms underlying immune evasion, and discusses the therapeutic potential of combined metabolic-immune intervention strategies.
Indexed as
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What 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.