ReviewAmerican journal of reproductive immunology (New York, N.Y. : 1989)2026
Natural Products Targeting Oxidative Stress-Inflammation Crosstalk in Endometriosis.
Review in American journal of reproductive immunology (New York, N.Y. : 1989), 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
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
1 citing paper in PubMed.
- Inflammation-Targeted Endometriosis Research Needs Pain, Mood, and Fertility-Priority Outcomes.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
problemEndometriosis is a chronic, estrogen-dependent inflammatory disorder marked by ectopic endometrial-like tissue growth, resulting in pelvic pain, infertility, and significant declines in quality of life. Despite extensive research, current therapies remain largely symptomatic and are often associated with recurrence, hormonal adverse effects, and compromised fertility outcomes. Growing evidence indicates that oxidative stress, chronic inflammation, mitochondrial dysfunction, altered immune surveillance and metabolic dysregulation are central drivers of lesion establishment and progression. However, these interconnected mechanisms are often examined in isolation, limiting translational progress. METHOD OF STUDY: We provide a comprehensive, integrative analysis of the molecular and cellular pathways underlying endometriosis, with particular emphasis on oxidative stress-inflammation crosstalk, signalling cascades supporting lesion survival, and emerging metabolic and mitochondrial targets. By critically synthesising recent experimental, preclinical, and clinical findings, this review highlights mechanistic overlaps that may explain therapeutic resistance and disease recurrence. Furthermore, it evaluates novel pharmacological and nutraceutical interventions targeting redox imbalance, inflammatory mediators, and intracellular signalling pathways, thereby expanding the conceptual framework beyond conventional hormonal suppression. Rising global endometriosis prevalence and its socioeconomic burden necessitate a shift from purely symptomatic management to mechanism-driven therapeutic strategies.
resultsThis review addresses that gap by consolidating dispersed evidence into a unified mechanistic perspective, identifying promising translational targets, and proposing future research directions. The insights provided will help in creating safer, fertility-preserving and more durable treatments. Thus, we categorise natural products by: (1) translational development stage (in vitro to clinical candidate); (2) regulatory pathway (dietary supplement, herbal medicine, or pharmaceutical); and (3) clinical context (e.g., pain control, recurrence prevention, or fertility preservation).
conclusionThis structured, clinically-oriented framework distinguishes the present synthesis from mechanistic reviews and serves to guide both future research design and rational integration of natural products into endometriosis therapeutic strategies.
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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.